33 results on '"Wenying, Song"'
Search Results
2. Comparison of Chemical Compositions and Antioxidant Activities for the Immature Fruits of Citrus changshan-huyou Y.B. Chang and Citrus aurantium L.
- Author
-
Qixin Zhang, Wenying Song, Guanqi Tao, Qin Li, Lixia Wang, Wenkang Huang, Lijuan Gao, Lai Yin, and Yiping Ye
- Subjects
Aurantii Fructus ,chemometric analysis ,chemical comparison ,Citrus aurantium L. ,Citrus changshan-huyou Y.B. Chang ,Quzhou Aurantii Fructus ,Organic chemistry ,QD241-441 - Abstract
Quzhou Aurantii Fructus (QAF), the dried immature fruit of Citrus changshan-huyou Y.B. Chang, is similar to Aurantii Fructus (AF), the dried immature fruit of Citrus aurantium L. or its cultivars, in terms of composition, pharmacological action, and appearance. However, potential chemical markers to distinguish QAF from AF remain unknown owing to the lack of a comprehensive systematic chemical comparison aligned with discriminant analysis. To achieve a better understanding of the differences in their composition, this study aimed to identify the basic chemical compounds in QAF (n = 42) and AF (n = 8) using ultra-performance liquid chromatography coupled with electron spray ionization and quadrupole time-of-flight mass spectrometry (UPLC−QTOF/MS) and gas chromatography coupled with mass spectrometry (GC−MS). Principal component analysis (PCA), orthogonal partial least squares-discriminant analysis (OPLS−DA), and hierarchical clustering analysis (HCA) were used to further analyze, screen, and verify potential chemical markers; the antioxidant capacity was assayed in vitro. A total of 108 compounds were found in QAF and AF, including 25 flavonoids, 8 limonoids, 2 coumarins, and 73 volatile components. The chemometric analysis indicated that the main components in QAF and AF were very similar. Trace differential components, including 9 flavonoids, 2 coumarins, 5 limonoids, and 26 volatile compounds, were screened as potential chemical markers to distinguish between QAF and AF. Additionally, the antioxidant capacity of QAF was found to be greater than that of AF. This research provides insights into the quality control and clinical application of QAF.
- Published
- 2023
- Full Text
- View/download PDF
3. Bridge Moving Load Recognition Based on Deep Learning.
- Author
-
Feng Gao, Shuri Cai, Hongxiang Guo, Wenying Song, Jinquan Zhang, Gang Liu, and Han Wei
- Published
- 2019
- Full Text
- View/download PDF
4. Bridge Apparent Damage Detection System Based on Deep Learning.
- Author
-
Wenying Song, Shuri Cai, Hongxiang Guo, Feng Gao, Jinquan Zhang, Gang Liu, and Han Wei
- Published
- 2019
- Full Text
- View/download PDF
5. MicroRNA-20b-5p regulates propofol-preconditioning-induced inhibition of autophagy in hypoxia-and-reoxygenation-stimulated endothelial cells
- Author
-
Zhen, Wang, Hui, Ding, Wenying, Song, and Yulong, Song
- Published
- 2020
- Full Text
- View/download PDF
6. Comparison of Chemical Compositions and Antioxidant Activities for the Immature Fruits of Citrus changshan-huyou Y.B. Chang and Citrus aurantium L
- Author
-
Ye, Qixin Zhang, Wenying Song, Guanqi Tao, Qin Li, Lixia Wang, Wenkang Huang, Lijuan Gao, Lai Yin, and Yiping
- Subjects
Aurantii Fructus ,chemometric analysis ,chemical comparison ,Citrus aurantium L ,Citrus changshan-huyou Y.B. Chang ,Quzhou Aurantii Fructus - Abstract
Quzhou Aurantii Fructus (QAF), the dried immature fruit of Citrus changshan-huyou Y.B. Chang, is similar to Aurantii Fructus (AF), the dried immature fruit of Citrus aurantium L. or its cultivars, in terms of composition, pharmacological action, and appearance. However, potential chemical markers to distinguish QAF from AF remain unknown owing to the lack of a comprehensive systematic chemical comparison aligned with discriminant analysis. To achieve a better understanding of the differences in their composition, this study aimed to identify the basic chemical compounds in QAF (n = 42) and AF (n = 8) using ultra-performance liquid chromatography coupled with electron spray ionization and quadrupole time-of-flight mass spectrometry (UPLC−QTOF/MS) and gas chromatography coupled with mass spectrometry (GC−MS). Principal component analysis (PCA), orthogonal partial least squares-discriminant analysis (OPLS−DA), and hierarchical clustering analysis (HCA) were used to further analyze, screen, and verify potential chemical markers; the antioxidant capacity was assayed in vitro. A total of 108 compounds were found in QAF and AF, including 25 flavonoids, 8 limonoids, 2 coumarins, and 73 volatile components. The chemometric analysis indicated that the main components in QAF and AF were very similar. Trace differential components, including 9 flavonoids, 2 coumarins, 5 limonoids, and 26 volatile compounds, were screened as potential chemical markers to distinguish between QAF and AF. Additionally, the antioxidant capacity of QAF was found to be greater than that of AF. This research provides insights into the quality control and clinical application of QAF.
- Published
- 2023
- Full Text
- View/download PDF
7. Retain the common ground: implications of research on fringe belt and urban green infrastructure for urban landscape revitalisation, a case of Quanzhou
- Author
-
Wenying Song
- Subjects
Geography, Planning and Development ,Management, Monitoring, Policy and Law ,Nature and Landscape Conservation ,General Environmental Science - Published
- 2022
8. The role of TLR4/MyD88/NF-κB in the protective effect of ulinastatin on intestinal mucosal barrier in mice with sepsis
- Author
-
Wenying Song, Huang Jing, Ying Li, and Hui Ding
- Abstract
Objective To investigate the effect of TLR4 /MyD88 /NF-κB signaling pathway in the protective effect of ulinastatin on intestinal mucosal barrier in mice with sepsis. Methods The mouse model of sepsis was established by classical cecal ligation and perforation. Thirty-two SPF C57BL/6 mice were randomly divided into four groups with 8 in each: control group (Con group), ulinastatin group (Uti group), Uti +TLR4 agonist LPS group (Uti+LPS group) and LPS group. Mice in the Con group received the same volume of saline injected into the tail vein 2 hours after modeling; Mice in the Uti group received 10000 U/kg ulinastatin injected into tail vein 2 hours after modeling; Mice in the Uti+LPS group received LPS (5mg/kg) injected into tail vein at 0h after modeling, other procedures were the same as in the Uti group; Mice in the LPS group received LPS (5mg/kg) injected into tail vein 0h after modeling. The weight loss ratio of mice was calculated at 48h after surgery. All animals were sacrificed at 48h after surgery to assess the injury of jejunal mucosa, the levels of TNF-α, IL-6 and IL-1 β in tail vein, and the expression of TLR4, MyD88 and NF-κ B mRNA in small intestinal mucosa tissues using ELASA and RT-PCR. Results The weight change of mice in Uti at 48h after operation was significantly reduced than that of the Con (p=0. 008 vs. Con); while the weight change of mice in Uti+LPS group and LPS group was significantly increased than that of the Uti (P=0. 020, P=0. 036 vs. Uti). The scores of intestinal mucosal injury at 48 h of the Uti were significantly lower than that of the Con (p<0.001 vs. Con);while the scores of intestinal mucosal injuryat 48 h of the Uti+LPS were significantly higher than that of the Uti ( P=0.044 vs. Uti). The expression of TNF-α, IL-6 and IL-1 β in the Uti decreased significantly at 48h after surgery than that in the Con(P=0.001,P=0.014,P=0.004 vs. Con), while the expression of TNF-α, IL-6 and IL-1β in Uti+LPS increased significantly at 48h after surgery than that in the Uti(P=0.026,P=0.040,P=0.039 vs. Uti). The expression of TLR4, MyD88 and NF-κB mRNA in Uti decreased significantly than that in the Con(P=0.001,P=0.021,P=0.007 vs. Con); while the expression of TLR4, MyD88 and NF-κB mRNA in Uti+LPS was higher than that in Uti (P=0.023,P=0.040,P=0.045 vs. Uti). Conclusion These findings indicate that the intestinal mucosal barrier protective effect against sepsis of ulinastatin may be mediated through the TLR4/MyD88/NF-κB pathway.
- Published
- 2023
9. An integrated spatial strategy for the inner fringe belt as an operational entity
- Author
-
Wenying Song
- Subjects
Urban Studies ,Archeology ,urban-morphology fringe-belt landscape-revitalisation - Published
- 2021
10. Retraction notice to <'Diverse signaling pathways through the SDF-1/CXCR4 chemokine axis in prostate cancer cell lines leads to altered patterns of cytokine secretion and angiogenesis'> <[Cellular Signaling 17/12 (2005) 1578–1592]>
- Author
-
Jincheng Wang, Wenying Song, Jacques E. Nör, Yanxi Sun, Jianhua Wang, Cun-Yu Wang, and Russell S. Taichman
- Subjects
medicine.medical_specialty ,Notice ,business.industry ,General surgery ,Published Erratum ,MEDLINE ,Medicine ,Cell Biology ,business - Published
- 2021
11. Loss of transforming growth factor-β1 in epithelium cells affects enamel formation in mice
- Author
-
Lili Xiang, Qing Chu, Wenying Song, Yanli Wang, Yan Gao, Yuguang Gao, Xu Zhenzhen, Yuehua Gao, and Congcong Qi
- Subjects
0301 basic medicine ,Mice, Transgenic ,Real-Time Polymerase Chain Reaction ,Transforming Growth Factor beta1 ,03 medical and health sciences ,Mice ,0302 clinical medicine ,stomatognathic system ,Conditional gene knockout ,Animals ,AMBN ,General Dentistry ,AMELX ,Enamel paint ,Chemistry ,Enamel Organ ,Epithelial Cells ,030206 dentistry ,Cell Biology ,General Medicine ,X-Ray Microtomography ,Enamel rod ,Cell biology ,stomatognathic diseases ,Enamel mineralization ,Disease Models, Animal ,030104 developmental biology ,Otorhinolaryngology ,visual_art ,visual_art.visual_art_medium ,Microscopy, Electron, Scanning ,Amelogenin ,Ameloblast - Abstract
Objectives In order to understand the specific in vivo function of transforming growth factor-beta1 (TGF-β1), we successfully established aTGF-β1 deficient mouse model using a conditional knockout method. In the present study, we aimed to further understand the potential role of TGF-β1 in enamel formation. Design Transgenic mice withoutTGF-β1 in epithelial cells were generated. Scanning electron microscopy and micro-computed tomography analysis were used to detect the dental appearance, enamel microstructure and tooth density. Histological analysis was used to examine the residual organic matrix of enamel. Quantitative real-time polymerase chain reaction was used to analyze the expressions of enamel matrix proteins at the mRNA level. Results The enamel of mandibular molars and incisors inTGF-β1 conditional knockout mice displayed severe attrition and lower density compared with the wild-type littermates. A slender microstructure of enamel rod was observed, and enamel matrix proteins were retained in the enamel space at the maturation stage in conditional knockout mice. Moreover, the expressions of enamel matrix protein-encoding genes, such as amelogenin (Amelx), ameloblastin (Ambn), Enamelin (Enam) and matrix metalloproteinase-20 (Mmp-20), were increased in enamel organs of conditional knockout mice. On the other hand, the expressions of Amelotin (Amtn), kallikrein-related peptidase-4 (Klk4), C4orf26 and WD repeat-containing protein 72 (Wdr72) were dramatically decreased at the transition and maturation stages. Conclusions TGF-β1 played an important role in enamel mineralization through decreasing synthesis ofAmelx, Ambn and Enam and increasing synthesis of Klk4, Amtn, Corf26 and Wdr72.
- Published
- 2018
12. Ablation of Runx2 in Ameloblasts Suppresses Enamel Maturation in Tooth Development
- Author
-
Zhiheng Dong, Xianhua Gao, Li Zhang, Lili Xiang, Qing Chu, Yuguang Gao, Mingyu Li, Wenying Song, Yan Gao, Yumin Wang, and Zhenzhen Xu
- Subjects
0301 basic medicine ,endocrine system ,lcsh:Medicine ,Core Binding Factor Alpha 1 Subunit ,Article ,03 medical and health sciences ,Gene Knockout Techniques ,Mice ,stomatognathic system ,Dental Enamel Proteins ,Conditional gene knockout ,Ameloblasts ,Animals ,AMBN ,lcsh:Science ,Dental Enamel ,AMELX ,Minerals ,Multidisciplinary ,Enamel paint ,Amelogenin ,Chemistry ,lcsh:R ,Enamel rod ,Cell biology ,stomatognathic diseases ,030104 developmental biology ,Gene Expression Regulation ,visual_art ,visual_art.visual_art_medium ,lcsh:Q ,Kallikreins ,ENAM ,Ameloblast - Abstract
Runt-related transcription factor 2 (Runx2) is involved in the early stage of tooth development. However, only few studies have reported the role of Runx2 in enamel development, which may be attributed to that Runx2 full knockout mice cannot survive after birth. In the present study, we successfully established a Runx2-deficient mouse model using a conditional knockout (cKO) method. We observed a significant reduction in the degree of mineralization and the decreased size of enamel rods in cKO mice. Histological analysis showed the retained enamel proteins in enamel layer at maturation stage in cKO molars. Further analysis by qRT-PCR revealed that the expressions of genes encoding enamel structure proteins, such as amelogenin (AMELX), ameloblastin (AMBN) and enamelin (ENAM), were increased in cKO enamel organs. On the other hand, the expression of kallikrein-related peptidase-4 (KLK4) at the mRNA and protein levels was dramatically decreased from late secretory stage to maturation stage in cKO enamel organs, while the expression of matrix metalloproteinase-20 (MMP-20) was not significantly altered. Finally, immunohistochemistry indicated that the uptake of amelogenins by ameloblasts was significantly decreased in cKO mice. Taken together, Runx2 played critical roles in controlling enamel maturation by increasing synthesis of KLK4 and decreasing synthesis of AMELX, AMBN and ENAM.
- Published
- 2018
13. Electroacupuncture Attenuates Cerebral Ischemia-Reperfusion Injury in Diabetic Mice Through Adiponectin Receptor 1-Mediated Phosphorylation of GSK-3β
- Author
-
Qiang Wang, Hong Yin, Feng Wang, Tao Jiang, Lize Xiong, Lixin Liu, Fan Guo, Wenying Song, Haidong Wei, and Lei Ma
- Subjects
Male ,medicine.medical_specialty ,Electroacupuncture ,medicine.medical_treatment ,Neuroscience (miscellaneous) ,Ischemia ,Neuroprotection ,Brain Ischemia ,Diabetes Mellitus, Experimental ,Glycogen Synthase Kinase 3 ,Mice ,Cellular and Molecular Neuroscience ,Internal medicine ,medicine ,Animals ,Phosphorylation ,GSK3B ,Adiponectin receptor 1 ,Glycogen Synthase Kinase 3 beta ,Adiponectin ,business.industry ,medicine.disease ,Streptozotocin ,Mice, Inbred C57BL ,Endocrinology ,Neurology ,Reperfusion Injury ,Receptors, Adiponectin ,business ,Reperfusion injury ,medicine.drug - Abstract
Diabetes mellitus substantially increases the risk of stroke and enhances brain's vulnerability to ischemia insult. Electroacupuncture (EA) pretreatment was proved to induce cerebral ischemic tolerance in normal stroke models. Whether EA could attenuate cerebral ischemia injury in diabetic mice and the possible underlying mechanism are still unrevealed. Male C57BL/6 mice were subjected to streptozotocin (STZ) for diabetic models. After inducing focal cerebral ischemia model, the levels of plasma and cerebral adiponectin (APN) were measured as well as the expression of cerebral adiponectin receptor 1 (AdipoR1) and 2 (AdipoR2). The neurobehavioral score, infarction volume, and cellular apoptosis were evaluated with or without AdipoR1 short interfering RNA (siRNA). The role of phosphorylation of glycogen synthesis kinase 3 beta (GSK-3β) at Ser-9 in the EA pretreatment was also assessed. EA pretreatment increased both plasma and cerebral APN levels and enhanced neuronal AdipoR1 in diabetic mice. In addition, EA reduced infarct size, improved neurological outcomes, and inhibited cell apoptosis after reperfusion. These beneficial effects were reversed by AdipoR1 knockdown. Furthermore, EA increased GSK-3β phosphorylation (p-GSK-3β) in the ipsilateral penumbra. Augmented p-GSK-3β induced neuroprotective effects similar to those of EA pretreatment. In contrast, dampened p-GSK-3β could reverse the neuroprotective effects of EA. In addition, the increase in p-GSK-3β by EA was abolished by AdipoR1 knockdown. We conclude that EA pretreatment increases the production of APN, which induce protective effects against cerebral ischemia-reperfusion injury through neuronal AdipoR1-mediated phosphorylation of GSK-3β in diabetic mice.
- Published
- 2014
14. Ischemic postconditioning protects the spinal cord from ischemia–reperfusion injury via modulation of redox signaling
- Author
-
Lize Xiong, Binxiao Su, Jing Sun, Hailong Dong, Rui Yang, and Wenying Song
- Subjects
Male ,Pulmonary and Respiratory Medicine ,Time Factors ,Ischemia ,Neuroprotection ,Antioxidants ,Drug Administration Schedule ,Gene Expression Regulation, Enzymologic ,Superoxide dismutase ,medicine ,Animals ,Ischemic Postconditioning ,chemistry.chemical_classification ,Paraplegia ,Reactive oxygen species ,biology ,business.industry ,Spinal Cord Ischemia ,Superoxide Dismutase ,Free Radical Scavengers ,medicine.disease ,Spinal cord ,Catalase ,Lumbar Spinal Cord ,Disease Models, Animal ,Oxidative Stress ,medicine.anatomical_structure ,chemistry ,Spinal Cord ,Anesthesia ,Reperfusion Injury ,biology.protein ,Ischemic preconditioning ,Surgery ,Rabbits ,business ,Reactive Oxygen Species ,Cardiology and Cardiovascular Medicine ,Reperfusion injury ,Oxidation-Reduction - Abstract
Background It is well known that ischemic postconditioning reduces ischemic–reperfusion injury, but the underlying mechanism is not fully understood. The current study investigated the role of reactive oxygen species–mediated upregulation of endogenous antioxidant enzymes in the generation of a protective effect induced by ischemic postconditioning against spinal cord reperfusion injury in the rabbit. Methods New Zealand White rabbits were randomly allocated to sham, ischemia–reperfusion, and postconditioning groups (3 cycles of 30 seconds of reperfusion and 30 seconds of occlusion during the onset of reperfusion). Spinal cord ischemia was induced by clamping the infrarenal abdominal aorta for 20 minutes in the ischemia–reperfusion and postconditioning groups. Forty-eight hours after reperfusion, the neurologic status of the lower limbs was assessed. Blood samples were collected for analysis of serum neuron-specific enolase levels, and the lumbar spinal cord segments (L5-7) were harvested for histopathologic and antioxidant enzyme activities and mRNA analysis with or without administration of N-2-mercaptopropionylglycine (an effective oxygen free radical scavenger) given at different reperfusion times. Results Continuous administration of N-2-mercaptopropionylglycine for 13 minutes, starting at 10 minutes before (but not 10 minutes after) the beginning of reperfusion, attenuated the neuroprotective effect of postconditioning against spinal cord ischemia and reversed the increase in activity of the antioxidant enzymes superoxide dismutase and catalase in spinal cord tissue subjected to ischemic postconditioning. Conclusions The results indicate that reactive oxygen species–triggered upregulation of endogenous antioxidant enzyme activities may be involved in the mechanism of neuroprotection of ischemic postconditioning.
- Published
- 2013
- Full Text
- View/download PDF
15. Overexpression of constitutively active MAP3K7 in ameloblasts causes enamel defects of mouse teeth
- Author
-
Jinping, Zhao, primary, Qing, Chu, additional, Wenying, Song, additional, Chunyan, Yang, additional, Lili, Xiang, additional, Yao, Shi, additional, Yumin, Wang, additional, Zhenzhen, Xu, additional, Li, Zhang, additional, and Yuguang, Gao, additional
- Published
- 2017
- Full Text
- View/download PDF
16. TREK1 activation mediates spinal cord ischemic tolerance induced by isoflurane preconditioning in rats
- Author
-
Hao Wu, Xin Yin, Xijing Zhang, Wenying Song, Haopeng Zhang, Hailong Dong, Xiao-mei Chen, Binxiao Su, and Lize Xiong
- Subjects
Male ,Ischemia ,Pharmacology ,Neuroprotection ,Rats, Sprague-Dawley ,Potassium Channels, Tandem Pore Domain ,Western blot ,medicine ,Animals ,Ischemic Preconditioning ,Neurons ,Isoflurane ,medicine.diagnostic_test ,Spinal Cord Ischemia ,business.industry ,General Neuroscience ,medicine.disease ,Spinal cord ,Potassium channel ,Rats ,Amiloride ,Neuroprotective Agents ,medicine.anatomical_structure ,Spinal Cord ,Reperfusion Injury ,Anesthesia ,Anesthetics, Inhalation ,business ,Reperfusion injury ,medicine.drug - Abstract
The aim of this study is to examine the role of one of the two-pore (2P) domain K(+) channels, TREK (TWIK-related K(+) channels, TREK)-1, mediated neuroprotection on spinal cord afforded by isoflurane preconditioning. In Experiment 1, male Sprague-Dawley rats were randomly assigned to control (Con) group, an isoflurane preconditioning (Iso) group, and sham group. Twenty-four hours after the last pretreatment, spinal cord ischemia was induced in Con and Iso groups. Neurobehavioral testing and histopathologic examination were performed after reperfusion. In Experiment 2, the expression of the TREK1 in the spinal cord was assessed by immunohistochemistry, Western blot and real-time polymerase chain reaction. In Experiment 3, Amiloride, a blocker of stretch-sensitive channels, was administered intraperitoneally immediately prior to each isoflurane preconditioning. Iso group showed a significant reductions in motor deficit index as well as increases in the number of normal neurons compared with the Con group. The expression of TREK1 protein and the level of mRNA after ischemia were higher in the rats of the Iso group than those in the Con group. Amiloride pretreatment abolished the protective effects of Iso preconditioning. These finding indicate that isoflurane preconditioning had a neuroprotective effect against spinal cord ischemia reperfusion injury. These effects may be mediated through the TREK1 pathway.
- Published
- 2012
17. Inhibition of mitochondrial permeability transition pore opening contributes to the neuroprotective effects of ischemic postconditioning in rats
- Author
-
Lize Xiong, Jing Sun, Wenying Song, Hailong Dong, Lichao Hou, Qi Luan, and Ke-Liang Xie
- Subjects
Male ,Programmed cell death ,Voltage-dependent anion channel ,Ischemia ,Infarction ,Atractyloside ,Pharmacology ,Mitochondrial Membrane Transport Proteins ,Neuroprotection ,Brain Ischemia ,Rats, Sprague-Dawley ,Random Allocation ,chemistry.chemical_compound ,Microscopy, Electron, Transmission ,Cyclosporin a ,medicine ,Animals ,cardiovascular diseases ,Ischemic Postconditioning ,Molecular Biology ,biology ,Mitochondrial Permeability Transition Pore ,business.industry ,General Neuroscience ,MPTP ,medicine.disease ,Mitochondria ,Rats ,Mitochondrial permeability transition pore ,chemistry ,Anesthesia ,Cyclosporine ,biology.protein ,Neurology (clinical) ,business ,Developmental Biology - Abstract
Ischemic postconditioning (IPost) has been shown to attenuate cerebral ischemia–reperfusion injury. However, the mechanism remains elusive. Because opening of the mitochondrial permeability transition pore (MPTP) is a crucial determinant of cell death after ischemia–reperfusion, we hypothesized that the neuroprotective effect of IPost may be associated with inhibition of MPTP opening. In part 1 of this study, pentobarbital-anesthetized rats subjected to middle cerebral artery occlusion for 90 min, followed by reperfusion for 72 h, were assigned to receive one of the following treatments: three cycles of IPost (15 s each), intracerebroventricular injection of saline (control), administration of the MPTP inhibitor cyclosporin A (CsA) (2 μmol/L, 15 μL) or its vehicle alcohol, administration of the MPTP opener atractyloside (Atr) (2 mmol/L, 15 μL), or IPost plus CsA/Atr treatment. Neurological deficit scores (NDS) and infarct volumes were assessed. Mitochondrial ultrastructure and swelling were also examined after reperfusion. In part 2, control and IPost groups underwent ischemia (90 min) and reperfusion (15 min). CsA and Atr groups were treated as described in part 1. Brain mitochondria were isolated after reperfusion and MPTP activity was evaluated. IPost or CsA treatment significantly improved NDS and reduced infarction volume, while Atr reversed the neuroprotective effects of IPost, and attenuated the decrease in mitochondrial swelling induced by IPost or CsA. Thus, inhibiting MPTP opening may play a crucial role in the neuroprotective effects of IPost, which may have potential clinical value against cerebral ischemia–reperfusion injury.
- Published
- 2012
18. Cancer gene therapy with iCaspase-9 transcriptionally targeted to tumor endothelial cells
- Author
-
Taocong Jin, Zhihong Dong, Wenying Song, Maria G. Mantellini, Jacques E. Nör, and Gabriel Núñez
- Subjects
Cancer Research ,Transcription, Genetic ,Angiogenesis ,Genetic Vectors ,Apoptosis ,Mice, SCID ,Biology ,Tacrolimus ,Article ,Adenoviridae ,Cell Line ,Viral vector ,Neovascularization ,Mice ,chemistry.chemical_compound ,Cell Line, Tumor ,Neoplasms ,medicine ,Animals ,Humans ,Promoter Regions, Genetic ,Molecular Biology ,Neovascularization, Pathologic ,Reverse Transcriptase Polymerase Chain Reaction ,Endothelial Cells ,Genetic Therapy ,Suicide gene ,Flow Cytometry ,medicine.disease ,Vascular Endothelial Growth Factor Receptor-2 ,Xenograft Model Antitumor Assays ,Head and neck squamous-cell carcinoma ,Caspase 9 ,Vascular endothelial growth factor ,chemistry ,Tumor progression ,Cancer research ,Molecular Medicine ,Sarcoma ,medicine.symptom - Abstract
Antiangiogenic therapies have shown varying results partly because each tumor type secretes a distinct panel of angiogenic factors to sustain its own microvascular network. In addition, recent evidence demonstrated that tumors develop resistance to antiangiogenic therapy by turning on alternate angiogenic pathways when one pathway is therapeutically inhibited. Here, we test the hypothesis that expression of a caspase-based artificial death switch in tumor-associated endothelial cells will disrupt tumor blood vessels and slow down tumor progression irrespective of tumor type. Adenoviral vectors expressing inducible Caspase-9 (iCaspase-9) under transcriptional regulation with the endothelial cell-specific vascular endothelial growth factor receptor-2 (VEGFR2) promoter (Ad-hVEGFR2-iCaspase-9) induced apoptosis of proliferating human dermal microvascular endothelial cells (HDMECs), but not human tumor cells (UM-SCC-17B, head and neck squamous cell carcinoma; HepG2, hepatocellular carcinoma; PC-3, prostate adenocarcinoma; SLK, Kaposi's sarcoma; MCF-7, breast adenocarcinoma). Notably, apoptosis was dependent upon activation of iCaspase-9 with the dimerizer drug AP20187. Local delivery of Ad-hVEGFR2-iCaspase-9 followed by intraperitoneal injection of AP20187 ablated tumor microvessels and inhibited xenografted tumor growth in all tumor models evaluated here. We conclude that a cancer gene therapy strategy based on a transcriptionally targeted viral vector expressing an inducible caspase allows for selective and controlled ablation of microvessels of histopathologically diverse tumor types.
- Published
- 2008
19. Therapeutic window of globular adiponectin against cerebral ischemia in diabetic mice: the role of dynamic alteration of adiponectin/adiponectin receptor expression
- Author
-
Haixing Zhong, Fan Guo, Lixin Liu, Wenying Song, Lize Xiong, Qiang Wang, and Rui Yang
- Subjects
Male ,endocrine system diseases ,Apoptosis ,CHOP ,Brain Ischemia ,Brain ischemia ,Mice ,eIF-2 Kinase ,immune system diseases ,RNA, Small Interfering ,Endoplasmic Reticulum Chaperone BiP ,Caspase 12 ,Heat-Shock Proteins ,Adiponectin receptor 1 ,Neurons ,Multidisciplinary ,Neuroprotective Agents ,Reperfusion Injury ,Adiponectin ,Receptors, Adiponectin ,Rosiglitazone ,medicine.drug ,Signal Transduction ,medicine.medical_specialty ,Ischemia ,Protein Serine-Threonine Kinases ,Neuroprotection ,Article ,Diabetes Mellitus, Experimental ,Internal medicine ,medicine ,Animals ,Humans ,Hypoglycemic Agents ,Injections, Intraventricular ,business.industry ,nutritional and metabolic diseases ,Membrane Proteins ,medicine.disease ,Mice, Inbred C57BL ,Endocrinology ,Diabetes Mellitus, Type 1 ,Gene Expression Regulation ,Thiazolidinediones ,business ,Reperfusion injury ,human activities ,Transcription Factor CHOP - Abstract
Recent studies have demonstrated that adiponectin (APN) attenuates cerebral ischemic/reperfusion via globular adiponectin (gAD). However, the therapeutic role of gAD in cerebral ischemic injury in type 1 diabetes mellitus (T1DM) remains unclear. Our results showed that gAD improved neurological scores and reduced the infarct volumes in the 8-week T1DM (T1DM-8W) mice, but not in the 2-week T1DM (T1DM-2W) mice. Moreover, the ischemic penumbra APN levels increased and peaked in T1DM-2W mice and reduced to normal in T1DM-8W mice, while the APN receptor 1 (AdipoR1) expression change was the opposite. Administration of rosiglitazone in T1DM-2W mice up-regulated the expression of AdipoR1 and restored the neuroprotection of gAD, while intracerebroventricular injection of AdipoR1 small interfering RNA (siRNA) in T1DM-8W mice reversed it. Furthermore, the expression of p-PERK, p-IRE1 and GRP78 were increased whereas the expressions of CHOP and cleaved caspase-12 as well as the number of apoptotic neurons were decreased after gAD treatment in T1DM-8W mice. These beneficial effects of gAD were reversed by pretreatment with AdipoR1 siRNA. These results demonstrated a dynamic dysfunction of APN/AdipoR1 accompanying T1DM progression. Interventions bolstering AdipoR1 expression during early stages and gAD supplementation during advanced stages may potentially reduce the cerebral ischemic injury in diabetic patients.
- Published
- 2014
20. Effect of lipopolysaccharides on vascular endothelial growth factor expression in mouse pulp cells and macrophages
- Author
-
Maria G. Mantellini, Tatiana M. Botero, Jacques E. Nör, Carl T. Hanks, and Wenying Song
- Subjects
Angiogenesis ,Biology ,Molecular biology ,Vascular endothelial growth factor ,Neovascularization ,Vascular endothelial growth factor A ,chemistry.chemical_compound ,stomatognathic system ,Downregulation and upregulation ,chemistry ,Cell culture ,Immunology ,medicine ,Pulp (tooth) ,Secretion ,medicine.symptom ,General Dentistry - Abstract
Vascular endothelial growth factor (VEGF), a potent pro-angiogenic factor, might regulate the neovascularization observed in the pulp of teeth with deep caries. The purpose of this in vitro study was to evaluate the effect of bacterial lipopolysaccharides (LPS) on VEGF expression in dental pulp cells. Mouse odontoblast-like cells (MDPC-23) or undifferentiated pulp cells (OD-21) were exposed to 0-20 microg ml-1Escherichia coli LPS or 0-80 microg ml-1Prevotella intermedia LPS. As controls, mouse macrophages or gingival fibroblasts were exposed to LPS, since these cells are known to secrete VEGF. The VEGF expression was evaluated by reverse transcriptase polymerase chain reaction or enzyme-linked immunosorbent assay. The baseline expression levels of VEGF protein were higher in MDPC-23 and OD-21 than in fibroblasts or macrophages. Vascular endothelial growth factor protein expression was upregulated in MDPC-23 and macrophages exposed to E. coli LPS, but not in OD-21 cells or fibroblasts. Higher concentrations of P. intermedia LPS were required to induce VEGF expression in MDPC-23 cells. Treatment with LPS did not affect VEGF expression at the mRNA level in any of the cells evaluated. These results demonstrate that bacterial LPS upregulates VEGF expression in odontoblast-like cells and macrophages, and suggest that the regulation of VEGF expression occurs primarily at a post-transcriptional level.
- Published
- 2003
21. Globular adiponectin elicits neuroprotection by inhibiting NADPH oxidase-mediated oxidative damage in ischemic stroke
- Author
-
Wenying Song, Hailong Dong, Qiang Wang, Fan Guo, Haidong Wei, Huaning Wang, Tingting Huo, Qianzi Yang, and Lize Xiong
- Subjects
Male ,Antioxidant ,medicine.medical_treatment ,Ischemia ,Caspase 3 ,Apoptosis ,Pharmacology ,Neuroprotection ,Antioxidants ,Brain Ischemia ,Superoxide dismutase ,chemistry.chemical_compound ,Mice ,medicine ,Animals ,Neurons ,NADPH oxidase ,Membrane Glycoproteins ,Adiponectin ,biology ,General Neuroscience ,Brain ,NADPH Oxidases ,medicine.disease ,Malondialdehyde ,Mice, Inbred C57BL ,Stroke ,Oxidative Stress ,Neuroprotective Agents ,Biochemistry ,chemistry ,Reperfusion Injury ,NADPH Oxidase 2 ,biology.protein - Abstract
Recent studies indicate that adiponectin can attenuate cerebral ischemic lesions via its functional area located in the C-terminal globular domain, which is called globular adiponectin (gAD). However, the mechanisms underlying this action remain unclear. In this study, we investigated the antioxidant properties of gAD during cerebral ischemia. Adult male C57BL/6 mice received an intracerebral injection of gAD with or without tetrabromocinnamic acid (TBCA, a NADPH oxidase activator). Mice were subjected to middle cerebral artery occlusion (MCAO) after gAD injection. Infarct volume, neurological function, the activity of antioxidant enzymes (superoxide dismutase [SOD], catalase), the content of malondialdehyde (MDA), and the expression of Bax, Bcl-2, cleaved caspase-3 and NADPH oxidase 2 (NOX2) were examined at 24h after MCAO. Infarct volume was attenuated in gAD-transduced mice when compared with mice in the MCAO group, with significant improvement in neurological function. In addition, neuronal apoptosis was attenuated, along with the expression of Bax/Bcl-2 and cleaved caspase 3. Furthermore, the activities of SOD and catalase increased, and the content of MDA reduced. However, TBCA blocked the effect of gAD on cerebral protection and its antioxidant abilities. Taken together, these results demonstrate that the neuroprotective action of gAD may result from the promotion of antioxidant capacity by inhibiting the NOX2 signaling system.
- Published
- 2013
22. M9, A Novel Region of Amino‐Nogo‐A, Attenuates Cerebral Ischemic Injury by Inhibiting NADPH Oxidase‐Derived Superoxide Production in Mice
- Author
-
Huiwen Wang, Weilin Jin, Qiang Wang, Yajing Mi, Xingchun Gou, Lize Xiong, Liya Li, Fan Guo, and Wenying Song
- Subjects
Nogo Proteins ,Ischemia ,Apoptosis ,Pharmacology ,medicine.disease_cause ,Neuroprotection ,Brain Ischemia ,chemistry.chemical_compound ,Mice ,Superoxides ,Physiology (medical) ,Medicine ,Animals ,Pharmacology (medical) ,chemistry.chemical_classification ,Reactive oxygen species ,NADPH oxidase ,biology ,Superoxide ,business.industry ,NADPH Oxidases ,Original Articles ,Malondialdehyde ,medicine.disease ,Peptide Fragments ,Mice, Inbred C57BL ,Psychiatry and Mental health ,Neuroprotective Agents ,chemistry ,Anesthesia ,Apocynin ,biology.protein ,tat Gene Products, Human Immunodeficiency Virus ,business ,Oxidative stress ,Myelin Proteins - Abstract
SUMMARY Aims: In acute stroke, neurological damage is due to oxidative stress and neuronal apoptotic death. This study investigated whether Nogo-A 290-562 residues region (M9), fused to the transduction domain of the HIV trans-activator (TAT) protein, is neuroprotective against cerebral ischemia and the mechanisms. Methods: Transient focal cerebral ischemia was induced by middle cerebral artery occlusion in male C57BL/6J mice. TAT-M9, its mutation or vehicle was applied via intraperitoneal injection at the onset of reperfusion. The neurobehavioral scores, infarction volumes, neuronal apoptosis, and the ratio of Bax/Bcl-2 were evaluated. Malondialdehyde (MDA), reactive oxygen species (ROS) levels, and NADPH oxidase activation were measured in the presence or absence of the NADPH oxidase inhibitor apocynin or activator tetrabromocinnamic acid (TBCA). Results: Immunofluorescence results confirmed that TAT-M9 was transduced into brain parenchyma, and it significantly improved neurological behavior, reduced infarct volumes, protected neuronal cells from apoptosis, inhibited activation of NADPH oxidase, and decreased MDA and ROS contents. Furthermore, apocynin imitated the beneficial effects of TAT-M9, while TBCA abolished them. Conclusions: Our results demonstrate that TAT-M9 administration attenuates cerebral ischemia by inhibiting NADPH oxidase-mediated oxidative damage and neuronal apoptosis in mice. TAT-M9 may be a potential treatment for cerebrovascular disease.
- Published
- 2013
23. Diverse signaling pathways through the SDF-1/CXCR4 chemokine axis in prostate cancer cell lines leads to altered patterns of cytokine secretion and angiogenesis
- Author
-
Jincheng Wang, Yanxi Sun, Russell S. Taichman, Wenying Song, Jianhua Wang, Cun-Yu Wang, and Jacques E. Nör
- Subjects
MAPK/ERK pathway ,Male ,Vascular Endothelial Growth Factor A ,Chemokine ,Receptors, CXCR4 ,Angiogenesis ,MAP Kinase Signaling System ,Mice, SCID ,Mice ,Phosphatidylinositol 3-Kinases ,Cell Movement ,Cell Line, Tumor ,LNCaP ,Animals ,Humans ,Neoplasm Metastasis ,Protein kinase B ,Angiostatins ,PI3K/AKT/mTOR pathway ,Tissue Inhibitor of Metalloproteinase-2 ,biology ,Neovascularization, Pathologic ,Interleukin-6 ,Prostatic Neoplasms ,Cell Biology ,Chemokine CXCL12 ,biology.protein ,Cancer research ,Cytokines ,Cytokine secretion ,RNA Interference ,Signal transduction ,Chemokines, CXC - Abstract
The establishment of metastatic bone lesions in prostate cancer (CaP) is a process partially dependent on angiogenesis. Previously we demonstrated that the stromal-derived factor-1 (SDF-1 or CXCL12)/CXCR4 chemokine axis is critical for CaP cell metastasis. In this investigation, cell lines were established in which CXCR4 expression was knocked down using siRNA technology. When CaP cells were co-transplanted with human vascular endothelial cells into SCID mice, significantly fewer human blood vessels were observed paralleling the reductions in CXCR4 levels. Likewise, the invasive behaviors of the CaP cells were inhibited in vitro. From these functional observations we explored angiogenic and signaling mechanisms generated following SDF-1 binding to CXCR4. Differential activation of the MEK/ERK and PI3K/AKT pathways that result in differential secretion IL-6, IL-8, TIMP-2 and VEGF were seen contingent on the cell type examined; VEGF and TIMP-2 expression in PC3 cells are dependent on AKT activation and ERK activation in LNCaP and LNCaP C4-2B cells leads to IL-6 or IL-8 secretion. At the same time, expression of angiostatin levels were inversely related to CXCR4 levels, and inhibited by SDF-1 stimulation. These data link the SDF-1/CXCR4 pathway to changes in angiogenic cytokines by different signaling mechanisms and, suggest that the delicate equilibrium between proangiogenic and antiangiogenic factors may be achieved by different signal transduction pathways to regulate the angiogenic phenotype of prostate cancers. Taken together, our results provide new information regarding expression of functional CXCR4 receptor-an essential role and potential mechanism of angiogenesis upon SDF-1 stimulation.
- Published
- 2005
24. Antiangiogenic gene therapy: disruption of neovascular networks mediated by inducible caspase-9 delivered with a transcriptionally targeted adenoviral vector
- Author
-
Q Sun, Zhihong Dong, Jacques E. Nör, Gabriel Núñez, David M. Spencer, and Wenying Song
- Subjects
Programmed cell death ,Angiogenesis ,Genetic enhancement ,Basic fibroblast growth factor ,Genetic Vectors ,Apoptosis ,Mice, SCID ,Adenoviridae ,chemistry.chemical_compound ,Mice ,Transduction, Genetic ,Neoplasms ,Genetics ,In Situ Nick-End Labeling ,Animals ,Humans ,Molecular Biology ,Caspase ,Skin ,Caspase-9 ,biology ,Neovascularization, Pathologic ,Microcirculation ,Endothelial Cells ,Genetic Therapy ,Suicide gene ,Immunohistochemistry ,Vascular Endothelial Growth Factor Receptor-2 ,Caspase 9 ,Vascular endothelial growth factor ,chemistry ,Caspases ,Models, Animal ,Cancer research ,biology.protein ,Molecular Medicine - Abstract
The activation of an inducible caspase (iCaspase-9) mediates apoptosis of neovascular endothelial cells, and overcomes the prosurvival effect of vascular endothelial growth factor or basic fibroblast growth factor. The potential utilization of direct activation of caspases as an antiangiogenic strategy for treatment of angiogenesis-dependent diseases (eg cancer) requires expression of the inducible caspase primarily in the tumor endothelium. The objective of this work was to develop and characterize a transcriptionally targeted adenoviral vector that mediates expression of iCaspase-9 specifically in neovascular endothelial cells. We observed that adenoviral vectors containing the human VEGFR2 promoter induced reporter gene expression primarily in proliferating human dermal microvascular endothelial cells (HDMEC). HDMEC transduced with recombinant adenoviral vectors containing iCaspase-9 under regulation of the VEGFR2 promoter (Ad-hVEGFR2-iCaspase-9) and exposed to a cell-permeable dimerizer drug (AP20187), presented higher caspase-3 activity and apoptosis than controls (Por = 0.05). Using the SCID Mouse Model of Human Angiogenesis, we observed that local delivery of Ad-hVEGFR2-iCaspase-9 followed by intraperitoneal injection of AP20187 resulted in endothelial cell apoptosis and local ablation of microvessels. We believe that this constitutes the first report of a transcriptionally targeted antiangiogenic adenoviral vector that mediates neovascular disruption upon activation of a caspase-based artificial death switch.
- Published
- 2004
25. Effect of lipopolysaccharides on vascular endothelial growth factor expression in mouse pulp cells and macrophages
- Author
-
Tatiana M, Botero, Maria G, Mantellini, Wenying, Song, Carl T, Hanks, and Jacques E, Nör
- Subjects
Lipopolysaccharides ,Vascular Endothelial Growth Factor A ,Analysis of Variance ,Lymphokines ,Odontoblasts ,Reverse Transcriptase Polymerase Chain Reaction ,Vascular Endothelial Growth Factors ,Macrophages ,Enzyme-Linked Immunosorbent Assay ,Endothelial Growth Factors ,Fibroblasts ,Cell Line ,Up-Regulation ,Mice ,Animals ,Intercellular Signaling Peptides and Proteins ,RNA, Messenger ,RNA Processing, Post-Transcriptional ,Dental Pulp - Abstract
Vascular endothelial growth factor (VEGF), a potent pro-angiogenic factor, might regulate the neovascularization observed in the pulp of teeth with deep caries. The purpose of this in vitro study was to evaluate the effect of bacterial lipopolysaccharides (LPS) on VEGF expression in dental pulp cells. Mouse odontoblast-like cells (MDPC-23) or undifferentiated pulp cells (OD-21) were exposed to 0-20 microg ml-1Escherichia coli LPS or 0-80 microg ml-1Prevotella intermedia LPS. As controls, mouse macrophages or gingival fibroblasts were exposed to LPS, since these cells are known to secrete VEGF. The VEGF expression was evaluated by reverse transcriptase polymerase chain reaction or enzyme-linked immunosorbent assay. The baseline expression levels of VEGF protein were higher in MDPC-23 and OD-21 than in fibroblasts or macrophages. Vascular endothelial growth factor protein expression was upregulated in MDPC-23 and macrophages exposed to E. coli LPS, but not in OD-21 cells or fibroblasts. Higher concentrations of P. intermedia LPS were required to induce VEGF expression in MDPC-23 cells. Treatment with LPS did not affect VEGF expression at the mRNA level in any of the cells evaluated. These results demonstrate that bacterial LPS upregulates VEGF expression in odontoblast-like cells and macrophages, and suggest that the regulation of VEGF expression occurs primarily at a post-transcriptional level.
- Published
- 2003
26. [The value of specific neuronal anti-Hu antibody in the early diagnosis of small cell lung cancer]
- Author
-
Gang, Wang, Qiming, Chen, Yan, Zhu, Daoping, Ke, Weidong, Qian, and Wenying, Song
- Subjects
Adult ,Male ,Neurons ,Lung Neoplasms ,Blotting, Western ,RNA-Binding Proteins ,Nerve Tissue Proteins ,ELAV-Like Protein 4 ,Middle Aged ,Prognosis ,Antibodies ,ELAV Proteins ,Biomarkers, Tumor ,Humans ,Female ,Carcinoma, Small Cell ,Aged ,Paraneoplastic Syndromes, Nervous System - Abstract
To evaluate the value of specific neuronal anti-Hu antibody in the early diagnosis of small cell lung cancer (SCLC).Ninety-eight patients with SCLC were included in the study. Specific neuronal anti-Hu antibody was detected by immunohistochemistry (the ABC method) and Western blot.The sera from 40% (32/80) of the patients in group A (without paraneoplastic syndrome of the nervous system) reacted with the frozen sections of human cerebra and were stained by indirect immunoperoxidase method at final dilutions of 1:1,000 to 1:8,000, while the sera from 89% of the patients (16/18) in group B (with paraneoplastic syndrome of the nervous system) reacted at final dilutions of 1:1,000 to 1:64,000. Western blot analysis revealed that the specific neuronal anti-Hu antibody was identified at several bands of approximately 35,000 approximately 40,000 with nuclear extracts, and at 40,000 with HuD clonal protein. The anti-Hu antibody was detected in only two patients from group A, but in 16 patients from group B. The antibody was not detected in sera from 32 normal human subjects.Specific neuronal anti-Hu antibody at high titers was detected in patients with SCLC not complicated with paraneoplastic syndrome of the nervous system. This antibody may be useful in the early diagnosis of SCLC.
- Published
- 2003
27. Ablation of microvessels in vivo upon dimerization of iCaspase-9
- Author
-
David M. Spencer, Wenying Song, Yuanming Hu, Jacques E. Nör, and Gabriel Núñez
- Subjects
Vascular Endothelial Growth Factor A ,Endothelium ,Angiogenesis ,Genetic Vectors ,Caspase 3 ,Apoptosis ,Endothelial Growth Factors ,Mice, SCID ,Tacrolimus ,Cell Line ,Mice ,Neoplasms ,Genetics ,medicine ,Animals ,Humans ,Molecular Biology ,Caspase ,Enzyme Precursors ,Lymphokines ,biology ,Neovascularization, Pathologic ,Vascular Endothelial Growth Factors ,Microcirculation ,Genetic Therapy ,Suicide gene ,Molecular biology ,Caspase 9 ,Cell biology ,Endothelial stem cell ,Enzyme Activation ,Vascular endothelial growth factor A ,medicine.anatomical_structure ,Retroviridae ,Caspases ,Models, Animal ,biology.protein ,Molecular Medicine ,Fibroblast Growth Factor 2 ,Endothelium, Vascular ,Dimerization ,Injections, Intraperitoneal - Abstract
Anti-angiogenic therapies based on targeted disruption of the tumor microvascular network have been proposed for cancer treatment. Inhibitors of the endothelial cell pro-survival pathway mediated by VEGF were shown to activate caspases and cause microvascular regression, but the efficacy of this strategy can be hindered by the engagement of redundant survival pathways. Alternatively, if direct activation of an apical pro-apoptotic caspase is sufficient to disrupt microvessels in vivo, such a strategy could potentially override upstream endothelial cell survival inputs and disrupt tumor neovascular networks. Here, we fused caspase-9 to a mutated FKBP12 domain to express an inducible caspase-9 molecule (iCaspase-9) that can be activated by a cell-permeable dimerizer drug, and transduced this construct into primary endothelial cells. We found that drug-induced dimerization of iCaspase-9 is sufficient to activate endogenous caspase-3 and trigger apoptosis even when endothelial cells are treated with the pro-survival factors VEGF or bFGF. A single intraperitoneal injection of the dimerizer drug induced apoptosis of endothelial cells expressing iCaspase-9 and elimination of human microvessels engineered in immunodeficient mice. These results demonstrate that the activation of iCaspase-9 disrupts microvessels in vivo, and suggest a novel anti-angiogenic strategy based on the expression and controlled activation of an inducible death gene in neovascular endothelial cells.
- Published
- 2001
28. Human colon cancer cells are capable of evading FasL-mediated apoptosis by Fas-receptor-independent mechanisms
- Author
-
William Feliciano, Qiong-Duan Chen, Wenying Song, John Y. Kao, Chuan-Min Chen, and Jian-Jun Chen
- Subjects
Human colon cancer ,Hepatology ,Apoptosis ,Cancer research ,Gastroenterology ,Biology ,Fas receptor ,Fas ligand - Published
- 2001
29. Expression of Fas ligand is not a main mechanism used by tumors to counteract antitumor immunity
- Author
-
Jian-Jun Chen, John Y. Kao, Qiong Duan Zheng, Wenying Song, and Chuan Min Chen
- Subjects
Programmed cell death ,Fas Ligand Protein ,Dose-Response Relationship, Immunologic ,Mice, Nude ,chemical and pharmacologic phenomena ,Inflammation ,Mice, SCID ,Biology ,Fas ligand ,Proinflammatory cytokine ,Mice ,Immune privilege ,Antibody Specificity ,Neoplasms ,Tumor Cells, Cultured ,medicine ,Animals ,Humans ,fas Receptor ,Membrane Glycoproteins ,Cell Death ,Immunity ,hemic and immune systems ,Fas receptor ,Cell culture ,Apoptosis ,Immunology ,Cancer research ,Female ,biological phenomena, cell phenomena, and immunity ,medicine.symptom - Abstract
The role of Fas ligand (FasL) in tumor immune privilege is controversial. In this study, 22 human tumor cell lines reported to be FasL+ were reevaluated by Western blot analysis, ELISA, and a functional assay. None of the cells lines expressed FasL. To assess whether human tumors express FasL in vivo, susceptibility to FasL-mediated killing was evaluated. About 75% of the 22 tumors tested were sensitive to FasL-mediated apoptosis, suggesting, therefore, that only about 25% could possibly express FasL. To investigate whether "FasL+" human tumor cells could suppress the proinflammatory effects of FasL in vivo, FasL transfectants were generated from two prototype "FasL+" tumor cell lines. The transfectants expressing FasL were rejected by SCID mice. In contrast, all the mice inoculated with parental tumor cells developed large tumors. These results suggested that human tumor cells that express FasL and resist both FasL-mediated apoptosis and inflammation are rare or nonexistant. We concluded that FasL expression is not a main mechanism that tumors use to counteract antitumor immunity.
- Published
- 2004
30. Electroacupuncture pretreatment inhibits NADPH oxidase-mediated oxidative stress in diabetic mice with cerebral ischemia.
- Author
-
Fan Guo, Wenying Song, Tao Jiang, Lixin Liu, Feng Wang, Haixing Zhong, Hong Yin, Qiang Wang, and Lize Xiong
- Subjects
- *
ELECTROACUPUNCTURE , *NADPH oxidase , *OXIDATIVE stress , *CEREBRAL ischemia , *LABORATORY mice , *PEOPLE with diabetes , *STREPTOZOTOCIN , *PREVENTION - Abstract
We investigated the protective effect of electroacupuncture (EA) on cerebral ischemic injury in diabetic mice, and explored the role of NADPH oxidase-mediated oxidative stress. Male C57BL/6 mice were injected streptozotocin to induce diabetes. The mice were pretreated with EA at acupoint "Baihui" for 30min. Two hours after the end of EA pretreatment, focal cerebral ischemia was induced following 24h reperfusion. The neurobehavioral scores and infarction volumes, malondialdehyde (MDA), reactive oxygen species (ROS), and activation of NADPH oxidase were determined in the presence or absence of the NADPH oxidase inhibitor apocynin or activator tetrabromocinnamic acid (TBCA). EA pretreatment reduced infarct size and improved neurological outcomes 24h after reperfusion in the diabetic mice. EA also decreased cerebral MDA and ROS levels compared with the control group, and inhibited the NADPH oxidase activation. The beneficial effects were abolished by TBCA while pretreatment with apocynin mimicked the neuroprotective and anti-oxidative effects of EA. Our results demonstrated that EA attenuated cerebral ischemic injury by inhibiting NAPDH oxidase-mediated oxidative damage in diabetic mice. These results suggest a novel mechanism of EA pretreatment-induced tolerance in diabetic cerebral ischemia. [ABSTRACT FROM AUTHOR]
- Published
- 2014
- Full Text
- View/download PDF
31. Human tumor cells do not express CD95 ligand (FasL)
- Author
-
John Y. Kao, Jian-Jun Chen, Qiong-Duan Zheng, Wenying Song, and Chuan-Min Chen
- Subjects
Human tumor ,Cd95 ligand ,Hepatology ,Chemistry ,Cancer research ,Gastroenterology ,Fas ligand - Published
- 2001
32. Activation of iCaspase-9 in neovessels inhibits oral tumor progression
- Author
-
Daniel E. Hall, Wenying Song, Kristy A. Warner, Zhihong Dong, Benjamin David Zeitlin, Matthew Stephen Pinsky, Jacques E. Nör, and Elisabeta Karl
- Subjects
0301 basic medicine ,Pathology ,medicine.medical_specialty ,Endothelium ,Angiogenesis ,Mice, SCID ,Biology ,Article ,Neovascularization ,Mice ,03 medical and health sciences ,0302 clinical medicine ,Cell Line, Tumor ,medicine ,Animals ,Humans ,Luciferases ,General Dentistry ,Cells, Cultured ,Mouth neoplasm ,Analysis of Variance ,Neovascularization, Pathologic ,030102 biochemistry & molecular biology ,030206 dentistry ,Suicide gene ,Caspase 9 ,Enzyme Activation ,medicine.anatomical_structure ,Tumor progression ,Cell culture ,Caspases ,Luminescent Measurements ,Cancer cell ,Carcinoma, Squamous Cell ,Mouth Neoplasms ,Endothelium, Vascular ,medicine.symptom ,Neoplasm Transplantation - Abstract
Tumors of the oral cavity are highly vascularized malignancies. Disruption of neovascular networks was shown to limit the access of nutrients and oxygen to tumor cells and inhibit tumor progression. Here, we evaluated the effect of the activation of an artificial death switch (iCaspase-9) expressed in neovascular endothelial cells on the progression of oral tumors. We used biodegradable scaffolds to co-implant human dermal microvascular endothelial cells stably expressing iCaspase-9 (HDMEC-iCasp9) with oral cancer cells expressing luciferase (OSCC3-luc or UM-SCC-17B-luc) in immunodeficient mice. Alternatively, untransduced HDMEC were co-implanted with oral cancer cells, and a transcriptionaly targeted adenovirus (Ad-VEGFR2-iCasp-9) was injected locally to deliver iCaspase-9 to neovascular endothelial cells. In vivo bioluminescence demonstrated that tumor progression was inhibited, and immunohistochemistry showed that microvessel density was decreased, when iCaspase-9 was activated in tumor-associated microvessels. We conclude that activation of iCaspase-9 in neovascular endothelial cells is sufficient to inhibit the progression of xenografted oral tumors.
33. A Comparison Between Propofol and Etomidate in Hysteroscopy on Effect of Postoperative Sedation and Cognitive Function in Elderly Patients
- Author
-
Wenying Song, Anesthesiologist
- Published
- 2014
Catalog
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.