28 results on '"Guo, Chang"'
Search Results
2. A handy method to remove bacterial contamination from fungal cultures.
- Author
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Xiao-Xiao Shi, Hai-Ping Qiu, Jiao-Yu Wang, Zhen Zhang, Yan-Li Wang, and Guo-Chang Sun
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Medicine ,Science - Abstract
Contamination control and removal are very important technical aspects of microbiological research. Bacterial contamination is very common in fungal cultures. Currently, the commonly used approach for inhibiting bacteria is antibiotic treatment; however, there are drawbacks to using antibiotics, including incomplete removal, limited antibacterial spectra, tendency toward recontamination, effects to fungal strains, and potential risks to the environment. Therefore, in the present work, we developed a new method for bacterial removal from fungi cultured on solid medium, the Cabin-Sequestering (CS) method, based on the different culture characteristics between fungi and bacteria. First, 3-5 mm round or square holes (the "cabin") are excavated on a solid medium plate. The fungal strain containing possible bacterial contamination is inoculated into the cabin. The cabin is then covered with a sterilized coverslip, followed by incubation at the appropriate temperature. After 7-10 days of culturing, fungal hyphae grow out along the edge of the coverslip; however, the contaminating bacteria cannot pass through the space formed between the medium and the coverslip and, thus, remain in the cabin. The newly grown fungal hyphae around the coverslip are re-inoculated into fresh culture plates, where they form bacteria-free fungal colonies. The CS method is easy handling, with a short experimental cycle and rare recontamination. When necessary, it can also be used in combination with antibiotics in bacterial removal operations.
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- 2019
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3. MicroRNA-377 regulates mesenchymal stem cell-induced angiogenesis in ischemic hearts by targeting VEGF.
- Author
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Zhili Wen, Wei Huang, Yuliang Feng, Wenfeng Cai, Yuhua Wang, Xiaohong Wang, Jialiang Liang, Mashhood Wani, Jing Chen, Pin Zhu, Ji-Mei Chen, Ronald W Millard, Guo-Chang Fan, and Yigang Wang
- Subjects
Medicine ,Science - Abstract
MicroRNAs have been appreciated in various cellular functions, including the regulation of angiogenesis. Mesenchymal-stem-cells (MSCs) transplanted to the MI heart improve cardiac function through paracrine-mediated angiogenesis. However, whether microRNAs regulate MSC induced angiogenesis remains to be clarified. Using microRNA microarray analysis, we identified a microRNA expression profile in hypoxia-treated MSCs and observed that among all dysregulated microRNAs, microRNA-377 was decreased the most significantly. We also validated that vascular endothelial growth factor (VEGF) is a target of microRNA-377 using dual-luciferase reporter assay and Western-blotting. Knockdown of endogenous microRNA-377 promoted tube formation in human umbilical vein endothelial cells. We then engineered rat MSCs with lentiviral vectors to either overexpress microRNA-377 (MSC miR-377) or knockdown microRNA-377 (MSC Anti-377) to investigate whether microRNA-377 regulated MSC-induced myocardial angiogenesis, using MSCs infected with lentiviral empty vector to serve as controls (MSC Null). Four weeks after implantation of the microRNA-engineered MSCs into the infarcted rat hearts, the vessel density was significantly increased in MSC Anti-377-hearts, and this was accompanied by reduced fibrosis and improved myocardial function as compared to controls. Adverse effects were observed in MSC miR-377-treated hearts, including reduced vessel density, impaired myocardial function, and increased fibrosis in comparison with MSC Null-group. These findings indicate that hypoxia-responsive microRNA-377 directly targets VEGF in MSCs, and knockdown of endogenous microRNA-377 promotes MSC-induced angiogenesis in the infarcted myocardium. Thus, microRNA-377 may serve as a novel therapeutic target for stem cell-based treatment of ischemic heart disease.
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- 2014
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4. An intragenic SRF-dependent regulatory motif directs cardiac-specific microRNA-1-1/133a-2 expression.
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Qi Li, Junli Guo, Xi Lin, Xiangsheng Yang, Yanlin Ma, Guo-Chang Fan, and Jiang Chang
- Subjects
Medicine ,Science - Abstract
Transcriptional regulation is essential for any gene expression including microRNA expression. MiR-1-1 and miR-133a-2 are essential microRNAs (miRs) involved in cardiac and skeletal muscle development and diseases. Early studies reveal two regulatory enhancers, an upstream and an intragenic, that direct the miR-1-1 and miR-133a-2 transcripts. In this study, we identify a unique serum response factor (SRF) binding motif within the enhancer through bioinformatic approaches. This motif is evolutionarily conserved and is present in a range of organisms from yeast, flies, to humans. We provide evidence to demonstrate that this regulatory motif is SRF-dependent in vitro by electrophoretic mobility shift assay, luciferase activity assay, and endogenous chromatin immunoprecipitation assay followed by DNA sequence confirmation, and in vivo by transgenic lacZ reporter mouse studies. Importantly, our transgenic mice indicate that this motif is indispensable for the expression of miR1-1/133a-2 in the heart, but not necessary in skeletal muscle, while the enhancer is sufficient for miR1-1/133a-2 gene expression in both tissues. The mutation of the motif alone completely abolishes miR-1-1/133a-2 gene expression in the animal heart, but not in the skeletal muscle. Our findings reveal an additional architecture of regulatory complex directing miR-1-1/133a-1 gene expression, and demonstrate how this intragenic enhancer differentially manages the expression of the two miRs in the heart and skeletal muscle, respectively.
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- 2013
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5. Toll-like receptor (TLR) 2 and TLR4 differentially regulate doxorubicin induced cardiomyopathy in mice.
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Yonggang Ma, Xiaowei Zhang, Huayan Bao, Su Mi, Wenfeng Cai, Huimin Yan, Qingqing Wang, Ziyan Wang, Jun Yan, Guo-Chang Fan, Merry L Lindsey, and Zhuowei Hu
- Subjects
Medicine ,Science - Abstract
Recent evidence indicates that toll-like receptor (TLR) 2 and 4 are involved in the pathogenesis of dilated cardiomyopathy (DCM), but the exact mechanisms of their actions have not been elucidated. We explored the therapeutic potential of blocking TLRs in mice with established cardiomyopathy. Cardiomyopathy was generated by a single intraperitoneal injection of doxorubicin (10 mg/kg). Two weeks later, the mice were treated with TLR2 or TLR4 neutralizing antibody. Blocking TLR2, but not TLR4, activity not only reduced mortality, but also attenuated doxorubicin-induced cardiac dysfunction by 20% and inhibited myocardial fibrosis. To determine the differential effects of blocking TLR2 and TLR4 in chronic cardiomyopathy, mice were injected with doxorubicin (3.5 mg/kg) once a week for 8 weeks, followed by treatment with TLR2 or TLR4 neutralizing antibody for 40 days. Blocking TLR2 activity blunted cardiac dysfunction by 13% and inhibited cardiac fibrosis, which was associated with a significant suppression of myocardial inflammation. The underlying mechanism involved interrupting the interaction of TLR2 with its endogenous ligands, resulting in attenuation of inflammation and fibrosis. In contrast, blocking TLR4 exacerbated cardiac dysfunction and fibrosis by amplifying inflammation and suppressing autophagy. Our studies demonstrate that TLR2 and TLR4 play distinct roles in the progression of doxorubicin-induced DCM. TLR4 activity is crucial for the resolution of inflammation and cardiac fibrosis, while blocking TLR2 activity has therapeutic potential for the treatment of DCM.
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- 2012
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6. Hsp20 functions as a novel cardiokine in promoting angiogenesis via activation of VEGFR2.
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Xiaowei Zhang, Xiaohong Wang, Hongyan Zhu, Evangelia G Kranias, Yaoliang Tang, Tianqing Peng, Jiang Chang, and Guo-Chang Fan
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Medicine ,Science - Abstract
Heat shock proteins (Hsps) are well appreciated as intrinsic protectors of cardiomyocytes against numerous stresses. Recent studies have indicated that Hsp20 (HspB6), a small heat shock protein, was increased in blood from cardiomyopathic hamsters. However, the exact source of the increased circulating Hsp20 and its potential role remain obscure. In this study, we observed that the circulating Hsp20 was increased in a transgenic mouse model with cardiac-specific overexpression of Hsp20, compared with wild-type mice, suggesting its origin from cardiomyocytes. Consistently, culture media harvested from Hsp20-overexpressing cardiomyocytes by Ad.Hsp20 infection contained an increased amount of Hsp20, compared to control media. Furthermore, we identified that Hsp20 was secreted through exosomes, independent of the endoplasmic reticulum-Golgi pathway. To investigate whether extracellular Hsp20 promotes angiogenesis, we treated human umbilical vein endothelial cells (HUVECs) with recombinant human Hsp20 protein, and observed that Hsp20 dose-dependently promoted HUVEC proliferation, migration and tube formation. Moreover, a protein binding assay and immunostaining revealed an interaction between Hsp20 and VEGFR2. Accordingly, stimulatory effects of Hsp20 on HUVECs were blocked by a VEGFR2 neutralizing antibody and CBO-P11 (a VEGFR inhibitor). These in vitro data are consistent with the in vivo findings that capillary density was significantly enhanced in Hsp20-overexpressing hearts, compared to non-transgenic hearts. Collectively, our findings demonstrate that Hsp20 serves as a novel cardiokine in regulating myocardial angiogenesis through activation of the VEGFR signaling cascade.
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- 2012
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7. Correction: A handy method to remove bacterial contamination from fungal cultures
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Shi, Xiao-Xiao, primary, Qiu, Hai-Ping, additional, Wang, Jiao-yu, additional, Zhang, Zhen, additional, Wang, Yan-Li, additional, and Sun, Guo-Chang, additional
- Published
- 2020
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8. A handy method to remove bacterial contamination from fungal cultures
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Shi, Xiao-Xiao, primary, Qiu, Hai-Ping, additional, Wang, Jiao-yu, additional, Zhang, Zhen, additional, Wang, Yan-Li, additional, and Sun, Guo-Chang, additional
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- 2019
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9. MicroRNA-377 regulates mesenchymal stem cell-induced angiogenesis in ischemic hearts by targeting VEGF
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Ji-Mei Chen, Jing Chen, Pin Zhu, Ronald W. Millard, Xiaohong Wang, Yigang Wang, Zhili Wen, Wei Huang, Yuliang Feng, Yuhua Wang, Guo-Chang Fan, Mashhood Wani, Jialiang Liang, and Wenfeng Cai
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Male ,Vascular Endothelial Growth Factor A ,Cell signaling ,Pathology ,Angiogenesis ,Myocardial Infarction ,lcsh:Medicine ,Signal transduction ,Pathology and Laboratory Medicine ,Biochemistry ,Rats, Sprague-Dawley ,chemistry.chemical_compound ,Animal Cells ,Medicine and Health Sciences ,Blood and Lymphatic System Procedures ,lcsh:Science ,3' Untranslated Regions ,Cells, Cultured ,Tube formation ,Gene knockdown ,Multidisciplinary ,Neovascularization, Pathologic ,Reverse Transcriptase Polymerase Chain Reaction ,Stem Cells ,MicroRNA Expression Profile ,VEGF signaling ,Cell Hypoxia ,3. Good health ,Vascular endothelial growth factor ,Vascular endothelial growth factor A ,Medical Microbiology ,Cardiovascular Diseases ,Echocardiography ,Viral Pathogens ,Gene Knockdown Techniques ,Cellular Types ,Pathogens ,Stem cell ,Research Article ,Cell biology ,medicine.medical_specialty ,Induced Pluripotent Stem Cells ,Blotting, Western ,Cardiology ,Neovascularization, Physiologic ,Surgical and Invasive Medical Procedures ,Mesenchymal Stem Cell Transplantation ,Microbiology ,Retroviruses ,Human Umbilical Vein Endothelial Cells ,medicine ,Animals ,Humans ,Microbial Pathogens ,Heart Failure ,Biology and life sciences ,business.industry ,Gene Expression Profiling ,Lentivirus ,Mesenchymal stem cell ,lcsh:R ,Mesenchymal Stem Cells ,MicroRNAs ,chemistry ,Cancer research ,RNA ,lcsh:Q ,business ,Stem Cell Transplantation - Abstract
MicroRNAs have been appreciated in various cellular functions, including the regulation of angiogenesis. Mesenchymal-stem-cells (MSCs) transplanted to the MI heart improve cardiac function through paracrine-mediated angiogenesis. However, whether microRNAs regulate MSC induced angiogenesis remains to be clarified. Using microRNA microarray analysis, we identified a microRNA expression profile in hypoxia-treated MSCs and observed that among all dysregulated microRNAs, microRNA-377 was decreased the most significantly. We also validated that vascular endothelial growth factor (VEGF) is a target of microRNA-377 using dual-luciferase reporter assay and Western-blotting. Knockdown of endogenous microRNA-377 promoted tube formation in human umbilical vein endothelial cells. We then engineered rat MSCs with lentiviral vectors to either overexpress microRNA-377 (MSC miR-377) or knockdown microRNA-377 (MSC Anti-377) to investigate whether microRNA-377 regulated MSC-induced myocardial angiogenesis, using MSCs infected with lentiviral empty vector to serve as controls (MSC Null). Four weeks after implantation of the microRNA-engineered MSCs into the infarcted rat hearts, the vessel density was significantly increased in MSC Anti-377-hearts, and this was accompanied by reduced fibrosis and improved myocardial function as compared to controls. Adverse effects were observed in MSC miR-377-treated hearts, including reduced vessel density, impaired myocardial function, and increased fibrosis in comparison with MSC Null-group. These findings indicate that hypoxia-responsive microRNA-377 directly targets VEGF in MSCs, and knockdown of endogenous microRNA-377 promotes MSC-induced angiogenesis in the infarcted myocardium. Thus, microRNA-377 may serve as a novel therapeutic target for stem cell-based treatment of ischemic heart disease.
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- 2014
10. Radiation Exposure Decreases the Quantity and Quality of Cardiac Stem Cells in Mice
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Luo, Lan, primary, Urata, Yoshishige, additional, Yan, Chen, additional, Hasan, Al Shaimaa, additional, Goto, Shinji, additional, Guo, Chang-Ying, additional, Tou, Fang-Fang, additional, Xie, Yucai, additional, and Li, Tao-Sheng, additional
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- 2016
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11. An intragenic SRF-dependent regulatory motif directs cardiac-specific microRNA-1-1/133a-2 expression
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Junli Guo, Guo-Chang Fan, Xi Lin, Xiangsheng Yang, Qi Li, Yanlin Ma, and Jiang Chang
- Subjects
lcsh:Medicine ,Mice, Transgenic ,Biology ,Cell Line ,03 medical and health sciences ,Mice ,Serum response factor ,microRNA ,Gene expression ,Transcriptional regulation ,Animals ,Electrophoretic mobility shift assay ,Enhancer ,lcsh:Science ,030304 developmental biology ,Regulation of gene expression ,0303 health sciences ,Multidisciplinary ,Myocardium ,030302 biochemistry & molecular biology ,lcsh:R ,Molecular biology ,MicroRNAs ,Serum Response Element ,Gene Expression Regulation ,Organ Specificity ,lcsh:Q ,Chromatin immunoprecipitation ,Myoblasts, Cardiac ,Research Article - Abstract
Transcriptional regulation is essential for any gene expression including microRNA expression. MiR-1-1 and miR-133a-2 are essential microRNAs (miRs) involved in cardiac and skeletal muscle development and diseases. Early studies reveal two regulatory enhancers, an upstream and an intragenic, that direct the miR-1-1 and miR-133a-2 transcripts. In this study, we identify a unique serum response factor (SRF) binding motif within the enhancer through bioinformatic approaches. This motif is evolutionarily conserved and is present in a range of organisms from yeast, flies, to humans. We provide evidence to demonstrate that this regulatory motif is SRF-dependent in vitro by electrophoretic mobility shift assay, luciferase activity assay, and endogenous chromatin immunoprecipitation assay followed by DNA sequence confirmation, and in vivo by transgenic lacZ reporter mouse studies. Importantly, our transgenic mice indicate that this motif is indispensable for the expression of miR1-1/133a-2 in the heart, but not necessary in skeletal muscle, while the enhancer is sufficient for miR1-1/133a-2 gene expression in both tissues. The mutation of the motif alone completely abolishes miR-1-1/133a-2 gene expression in the animal heart, but not in the skeletal muscle. Our findings reveal an additional architecture of regulatory complex directing miR-1-1/133a-1 gene expression, and demonstrate how this intragenic enhancer differentially manages the expression of the two miRs in the heart and skeletal muscle, respectively.
- Published
- 2013
12. MicroRNA-377 Regulates Mesenchymal Stem Cell-Induced Angiogenesis in Ischemic Hearts by Targeting VEGF
- Author
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Wen, Zhili, primary, Huang, Wei, additional, Feng, Yuliang, additional, Cai, Wenfeng, additional, Wang, Yuhua, additional, Wang, Xiaohong, additional, Liang, Jialiang, additional, Wani, Mashhood, additional, Chen, Jing, additional, Zhu, Pin, additional, Chen, Ji-Mei, additional, Millard, Ronald W., additional, Fan, Guo-Chang, additional, and Wang, Yigang, additional
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- 2014
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13. Identification of Genes Preferentially Expressed by Highly Virulent Piscine Streptococcus agalactiae upon Interaction with Macrophages
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Guo, Chang-Ming, primary, Chen, Rong-Rong, additional, Kalhoro, Dildar Hussain, additional, Wang, Zhao-Fei, additional, Liu, Guang-Jin, additional, Lu, Cheng-Ping, additional, and Liu, Yong-Jie, additional
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- 2014
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14. NOS2 Is Critical to the Development of Emphysema in Sftpd Deficient Mice but Does Not Affect Surfactant Homeostasis
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Knudsen, Lars, primary, Atochina-Vasserman, Elena N., additional, Guo, Chang-Jiang, additional, Scott, Pamela A., additional, Haenni, Beat, additional, Beers, Michael F., additional, Ochs, Matthias, additional, and Gow, Andrew J., additional
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- 2014
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15. An Intragenic SRF-Dependent Regulatory Motif Directs Cardiac-Specific microRNA-1-1/133a-2 Expression
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Li, Qi, primary, Guo, Junli, additional, Lin, Xi, additional, Yang, Xiangsheng, additional, Ma, Yanlin, additional, Fan, Guo-Chang, additional, and Chang, Jiang, additional
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- 2013
- Full Text
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16. An Integrative Proteomics and Interaction Network-Based Classifier for Prostate Cancer Diagnosis
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Guo-Chang Chen, Hui-chan He, Deng-Liang Yang, Ru-Jun Mo, Wei-de Zhong, Funeng Jiang, Wen-Liang Zhou, Yanqiong Zhang, Yun-Xin Zhu, Sheng-bang Yang, Yan-Ru Chen, and Jiehong Huang
- Subjects
Proteomics ,Male ,Microarrays ,Gene Expression ,lcsh:Medicine ,Histone Deacetylase 1 ,Disease ,Bioinformatics ,Protein expression ,Prostate cancer ,Pathology ,Protein Interaction Maps ,lcsh:Science ,Aged, 80 and over ,Multidisciplinary ,Systems Biology ,Prostate Cancer ,Cancer Risk Factors ,Prostate Diseases ,RNA-Binding Proteins ,Genomics ,Middle Aged ,Oncology ,Medicine ,Immunohistochemical Analysis ,Research Article ,Urology ,Immunology ,Biology ,Molecular Genetics ,Diagnostic Medicine ,Interaction network ,Cancer Detection and Diagnosis ,Early Detection ,Biomarkers, Tumor ,medicine ,Humans ,PTB-Associated Splicing Factor ,Aged ,lcsh:R ,PTEN Phosphohydrolase ,Computational Biology ,Cancers and Neoplasms ,Prostatic Neoplasms ,Reproducibility of Results ,Diagnostic marker ,medicine.disease ,Genitourinary Tract Tumors ,Protein Interaction Networks ,Immunologic Techniques ,lcsh:Q ,Genome Expression Analysis ,Classifier (UML) ,Biomarkers ,General Pathology - Abstract
Aim Early diagnosis of prostate cancer (PCa), which is a clinically heterogeneous-multifocal disease, is essential to improve the prognosis of patients. However, published PCa diagnostic markers share little overlap and are poorly validated using independent data. Therefore, we here developed an integrative proteomics and interaction network-based classifier by combining the differential protein expression with topological features of human protein interaction networks to enhance the ability of PCa diagnosis. Methods and Results By two-dimensional fluorescence difference gel electrophoresis (2D-DIGE) coupled with MS using PCa and adjacent benign tissues of prostate, a total of 60 proteins with the differential expression in PCa tissues were identified as the candidate markers. Then, their networks were analyzed by GeneGO Meta-Core software and three hub proteins (PTEN, SFPQ and HDAC1) were chosen. After that, a PCa diagnostic classifier was constructed by support vector machine (SVM) modeling based on the microarray gene expression data of the genes which encode the hub proteins mentioned above. Validations of diagnostic performance showed that this classifier had high predictive accuracy (85.96∼90.18%) and area under ROC curve (approximating 1.0). Furthermore, the clinical significance of PTEN, SFPQ and HDAC1 proteins in PCa was validated by both ELISA and immunohistochemistry analyses. More interestingly, PTEN protein was identified as an independent prognostic marker for biochemical recurrence-free survival in PCa patients according to the multivariate analysis by Cox Regression. Conclusions Our data indicated that the integrative proteomics and interaction network-based classifier which combines the differential protein expression and topological features of human protein interaction network may be a powerful tool for the diagnosis of PCa. We also identified PTEN protein as a novel prognostic marker for biochemical recurrence-free survival in PCa patients.
- Published
- 2013
17. Association of SNP Rs6903956 on Chromosome 6p24.1 with Angiographical Characteristics of Coronary Atherosclerosis in a Chinese Population
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Guo, Chang-Yan, primary, Gu, Yan, additional, Li, Li, additional, Jia, En-Zhi, additional, Li, Chun-Jian, additional, Wang, Lian-Sheng, additional, Yang, Zhi-Jian, additional, Cao, Ke-Jiang, additional, and Ma, Wen-Zhu, additional
- Published
- 2012
- Full Text
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18. A Novel Viral SOCS from Infectious Spleen and Kidney Necrosis Virus: Interacts with Jak1 and Inhibits IFN-α Induced Stat1/3 Activation
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Guo, Chang-Jun, primary, Yang, Li-Shi, additional, Zhang, Ying-Fen, additional, Wu, Yan-Yan, additional, Weng, Shao-Ping, additional, Yu, Xiao-Qiang, additional, and He, Jian-Guo, additional
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- 2012
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19. Hsp20 Functions as a Novel Cardiokine in Promoting Angiogenesis via Activation of VEGFR2
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Zhang, Xiaowei, primary, Wang, Xiaohong, additional, Zhu, Hongyan, additional, Kranias, Evangelia G., additional, Tang, Yaoliang, additional, Peng, Tianqing, additional, Chang, Jiang, additional, and Fan, Guo-Chang, additional
- Published
- 2012
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20. Time Distribution of the Onset of Chest Pain in Subjects with Acute ST-Elevation Myocardial Infarction: An Eight-Year, Single-Center Study in China
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Jia, En-Zhi, primary, Xu, Zhen-Xia, additional, Cai, Hong-Zhou, additional, Guo, Chang–Yan, additional, Li, Li, additional, Zhu, Tie-Bing, additional, Wang, Lian-Sheng, additional, Cao, Ke-Jiang, additional, Ma, Wen-Zhu, additional, and Yang, Zhi-Jian, additional
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- 2012
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21. Combined Effects of Admission Serum Creatinine Concentration with Age and Gender on the Prognostic Significance of Subjects with Acute ST-Elevation Myocardial Infarction in China.
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Li, Zhao-Yang, Pu-Liu, Chen, Zhao-Hong, An, Feng-Hui, Li, Li-Hua, Li-Li, Guo, Chang-Yan, Gu, Yan, Liu, Zhe, Zhu, Tie-Bing, Wang, Lian-Sheng, Li, Chun-Jian, Kong, Xiang-Qing, Ma, Wen-Zhu, Yang, Zhi-Jian, and Jia, En-Zhi
- Subjects
MYOCARDIAL infarction ,CREATININE ,SERUM ,REGRESSION analysis ,KIDNEY diseases ,PROGNOSIS - Abstract
Objective: to explore the impact of admission serum creatinine concentration on the in-hospital mortality and its interaction with age and gender in patients with acute ST-segment elevation myocardial infarction (STEMI) in China. Methods: 1424 acute STEMI patients were enrolled in the study. Anthropometric and laboratory measurements were collected from every patient. A Cox proportional hazards regression model was used to determine the relationships between the admission serum creatinine level (Cr level), age, sex and the in-hospital mortality. A crossover analysis and a stratified analysis were used to determine the combined impact of Cr levels with age and gender. Results: Female (HR 1.687, 95%CI 1.051∼2.708), elevated Cr level (HR 5.922, 95%CI 3.780∼9,279) and old age (1.692, 95%CI 1.402∼2.403) were associated with a high risk of death respectively. After adjusting for other confounders, the renal dysfunction was still independently associated with a higher risk of death (HR 2.48, 95% CI 1.32∼4.63), while female gender (HR 1.19, 95%CI 0.62∼2.29) and old age (HR 1.77, 95%CI 0.92∼3.37) was not. In addition, crossover analysis revealed synergistic effects between elevated Cr level and female gender (SI = 3.01, SIM = 2.10, AP = 0.55). Stratified analysis showed that the impact of renal dysfunction on in-hospital mortality was more pronounced in patients <60 years old (odds ratios 11.10, 95% CI 3.72 to 33.14) compared with patients 60 to 74 years old (odds ratios 5.18, 95% CI 2.48∼10.83) and patients ≥75years old (odds ratios 3.99, 95% CI 1.89 to 8.42). Conclusion: Serum Cr concentration on admission was a strong predictor for in-hospital mortality among Chinese acute STEMI patients especially in the young and the female. [ABSTRACT FROM AUTHOR]
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- 2014
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22. Identification of Genes Preferentially Expressed by Highly Virulent Piscine Streptococcus agalactiae upon Interaction with Macrophages.
- Author
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Guo, Chang-Ming, Chen, Rong-Rong, Kalhoro, Dildar Hussain, Wang, Zhao-Fei, Liu, Guang-Jin, Lu, Cheng-Ping, and Liu, Yong-Jie
- Subjects
- *
STREPTOCOCCUS agalactiae , *MACROPHAGES , *IN vitro studies , *BRAIN damage , *GENE expression in mammals , *VETERINARY medicine , *LABORATORY mice - Abstract
Streptococcus agalactiae, long recognized as a mammalian pathogen, is an emerging concern with regard to fish. In this study, we used a mouse model and in vitro cell infection to evaluate the pathogenetic characteristics of S. agalactiae GD201008-001, isolated from tilapia in China. This bacterium was found to be highly virulent and capable of inducing brain damage by migrating into the brain by crossing the blood–brain barrier (BBB). The phagocytosis assays indicated that this bacterium could be internalized by murine macrophages and survive intracellularly for more than 24 h, inducing injury to macrophages. Further, selective capture of transcribed sequences (SCOTS) was used to investigate microbial gene expression associated with intracellular survival. This positive cDNA selection technique identified 60 distinct genes that could be characterized into 6 functional categories. More than 50% of the differentially expressed genes were involved in metabolic adaptation. Some genes have previously been described as associated with virulence in other bacteria, and four showed no significant similarities to any other previously described genes. This study constitutes the first step in further gene expression analyses that will lead to a better understanding of the molecular mechanisms used by S. agalactiae to survive in macrophages and to cross the BBB. [ABSTRACT FROM AUTHOR]
- Published
- 2014
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23. NOS2 Is Critical to the Development of Emphysema in Sftpd Deficient Mice but Does Not Affect Surfactant Homeostasis.
- Author
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Knudsen, Lars, Atochina-Vasserman, Elena N., Guo, Chang-Jiang, Scott, Pamela A., Haenni, Beat, Beers, Michael F., Ochs, Matthias, and Gow, Andrew J.
- Subjects
DRUG development ,NITRIC-oxide synthases ,PULMONARY surfactant-associated protein D ,PULMONARY emphysema ,HOMEOSTASIS ,LABORATORY mice ,PROTEIN deficiency ,PATHOLOGICAL physiology - Abstract
Rationale: Surfactant protein D (SP-D) has important immuno-modulatory properties. The absence of SP-D results in an inducible NO synthase (iNOS, coded by NOS2 gene) related chronic inflammation, development of emphysema-like pathophysiology and alterations of surfactant homeostasis. Objective: In order to test the hypothesis that SP-D deficiency related abnormalities in pulmonary structure and function are a consequence of iNOS induced inflammation, we generated SP-D and iNOS double knockout mice (DiNOS). Methods: Structural data obtained by design-based stereology to quantify the emphysema-like phenotype and disturbances of the intracellular surfactant were correlated to invasive pulmonary function tests and inflammatory markers including activation markers of alveolar macrophages and compared to SP-D (Sftpd
−/− ) and iNOS single knockout mice (NOS2−/− ) as well as wild type (WT) littermates. Measurements and Results: DiNOS mice had reduced inflammatory cells in BAL and BAL-derived alveolar macrophages showed an increased expression of markers of an alternative activation as well as reduced inflammation. As evidenced by increased alveolar numbers and surface area, emphysematous changes were attenuated in DiNOS while disturbances of the surfactant system remained virtually unchanged. Sftpd−/− demonstrated alterations of intrinsic mechanical properties of lung parenchyma as shown by reduced stiffness and resistance at its static limits, which could be corrected by additional ablation of NOS2 gene in DiNOS. Conclusion: iNOS related inflammation in the absence of SP-D is involved in the emphysematous remodeling leading to a loss of alveoli and associated alterations of elastic properties of lung parenchyma while disturbances of surfactant homeostasis are mediated by different mechanisms. [ABSTRACT FROM AUTHOR]- Published
- 2014
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24. Stomatin-like protein 2 deficiency results in impaired mitochondrial translation
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Orsolya Lapohos, Woranontee Weraarpachai, Panagiotis Mitsopoulos, Hana Antonicka, Yu-Han Chang, Joaquín Madrenas, and Fan, Guo-Chang
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0301 basic medicine ,Sucrose ,Mitochondrial translation ,T-Lymphocytes ,lcsh:Medicine ,Gene Expression ,Lymphocyte Activation ,Disaccharides ,Biochemistry ,Mice ,White Blood Cells ,0302 clinical medicine ,Animal Cells ,Materials Physics ,Medicine and Health Sciences ,Enzyme-Linked Immunoassays ,lcsh:Science ,Inner mitochondrial membrane ,Energy-Producing Organelles ,Mice, Knockout ,Multidisciplinary ,T Cells ,Organic Compounds ,Physics ,Mitochondrial DNA ,Mitochondria ,Nucleic acids ,Chemistry ,mitochondrial fusion ,Mitochondrial Membranes ,Physical Sciences ,ATP–ADP translocase ,Cellular Structures and Organelles ,Cellular Types ,Sedimentation ,Research Article ,General Science & Technology ,Forms of DNA ,1.1 Normal biological development and functioning ,Knockout ,Immune Cells ,Immunology ,Materials Science ,Carbohydrates ,Nerve Tissue Proteins ,Biology ,Bioenergetics ,Research and Analysis Methods ,Mitochondrial Proteins ,03 medical and health sciences ,Underpinning research ,Genetics ,Animals ,Immunoassays ,Mitochondrial ribosome assembly ,Blood Cells ,lcsh:R ,Organic Chemistry ,Chemical Compounds ,Membrane Proteins ,Biology and Life Sciences ,Polypeptides ,Cell Biology ,DNA ,Mitochondrial carrier ,030104 developmental biology ,Protein Biosynthesis ,Translocase of the inner membrane ,DNAJA3 ,Immunologic Techniques ,lcsh:Q ,Protein Translation ,Generic health relevance ,Peptides ,030217 neurology & neurosurgery - Abstract
Mitochondria translate the RNAs for 13 core polypeptides of respiratory chain and ATP synthase complexes that are essential for the assembly and function of these complexes. This process occurs in close proximity to the mitochondrial inner membrane. However, the mechanisms and molecular machinery involved in mitochondrial translation are not fully understood, and defects in this process can result in severe diseases. Stomatin-like protein (SLP)-2 is a mainly mitochondrial protein that forms cardiolipin- and prohibitin-enriched microdomains in the mitochondrial inner membrane that are important for the formation of respiratory supercomplexes and their function. Given this regulatory role of SLP-2 in processes closely associated with the mitochondrial inner membrane, we hypothesized that the function of SLP-2 would have an impact on mitochondrial translation. 35S-Methionine/cysteine pulse labeling of resting or activated T cells from T cell-specific Slp-2 knockout mice showed a significant impairment in the production of several mitochondrial DNA-encoded polypeptides following T cell activation, including Cytb, COXI, COXII, COXIII, and ATP6. Measurement of mitochondrial DNA stability and mitochondrial transcription revealed that this impairment was at the post-transcriptional level. Examination of mitochondrial ribosome assembly showed that SLP-2 migrated in sucrose-density gradients similarly to the large ribosomal subunit but that its deletion at the genetic level did not affect mitochondrial ribosome assembly. Functionally, the impairment in mitochondrial translation correlated with decreased interleukin-2 production in activated T cells. Altogether, these data show that SLP-2 acts as a general regulator of mitochondrial translation.
- Published
- 2017
25. Shift toward greater pathologic post-myocardial infarction remodeling with loss of the adaptive hypertrophic signaling of alpha1 adrenergic receptors in mice
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Yanying Fan, Paul C. Simpson, Che-Chung Yeh, Michael J. Mann, Yanchun Xu, Yi-Lin Yang, and Fan, Guo-Chang
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Male ,0301 basic medicine ,Captopril ,Physiology ,Arbitrary unit ,Myocardial Infarction ,lcsh:Medicine ,Adrenergic ,Apoptosis ,Angiotensin-Converting Enzyme Inhibitors ,030204 cardiovascular system & hematology ,Cardiovascular ,Muscle hypertrophy ,Mice ,0302 clinical medicine ,Cell Signaling ,Fibrosis ,Receptors ,Medicine and Health Sciences ,2.1 Biological and endogenous factors ,Aetiology ,lcsh:Science ,Receptor ,Mice, Knockout ,Multidisciplinary ,Cell Death ,Ventricular Remodeling ,Heart ,alpha-1 ,Signaling Cascades ,3. Good health ,Heart Disease ,Cell Processes ,Anatomy ,Receptor Physiology ,Research Article ,Signal Transduction ,Cell Physiology ,medicine.medical_specialty ,MAPK signaling cascades ,Adrenergic receptor ,MAP Kinase Signaling System ,General Science & Technology ,Knockout ,Cardiology ,Stress Signaling Cascade ,03 medical and health sciences ,Receptors, Adrenergic, alpha-1 ,Internal medicine ,medicine ,Animals ,Ventricular remodeling ,Heart Disease - Coronary Heart Disease ,Physiological Adaptation ,Pressure overload ,business.industry ,Myocardium ,lcsh:R ,Biology and Life Sciences ,Cell Biology ,medicine.disease ,030104 developmental biology ,Endocrinology ,Cardiovascular Anatomy ,lcsh:Q ,Physiological Processes ,business - Abstract
Author(s): Yeh, Che-Chung; Fan, Yanying; Xu, Yanchun; Yang, Yi-Lin; Simpson, Paul C; Mann, Michael J | Abstract: RationaleWe have hypothesized that post-infarction cardiac remodeling can be influenced by shifts in the balance between intracellular mediators of "pathologic" and "physiologic" hypertrophy. Although alpha1 adrenergic receptors (alpha1-ARs) mediate pro-adaptive hypertrophy during pressure overload, little is known about their role or downstream mediators after myocardial infarction.MethodsWe performed loss-of-function experiments via coronary ligation in alpha1A-AR knockout (AKO) mice. Post-myocardial infarction (MI) remodeling was evaluated via echocardiography, quantitative reverse transcription-polymerase chain reaction (RT-PCR) analysis of cardiac fetal gene expression, histologic analysis of myocyte size, post-MI fibrosis and apoptosis, and Western blot analysis of apoptotic regulators.ResultsAlpha1A-AR knockout paradoxically increased post-MI hypertrophy compared to wild type controls (WT), but also increased ventricular dilatation, fibrosis, apoptosis, and 4-week post-MI mortality (64% in AKO vs. 25% in WT, P = 0.02), suggesting a shift toward greater pathologic hypertrophy in the absence of pro-adaptive alpha1A effects. alpha1A-AR knockout increased phospho-p38 levels in the pre-MI myocardium compared to WT (0.55 ± 0.16 vs. 0.03 ± 0.01, Pl0.05) but decreased phospho-ERK1/2 post-MI (0.49 ± 0.35 arbitrary units vs. 1.55 ± 0.43 in WT, Pl0.05). Furthermore, expression of pro-apoptotic factor Bax was increased (1.19 ± 0.15 vs. 0.78 ± 0.08, Pl0.05) and expression of anti-apoptotic factors Bcl2 was decreased (0.26 ± 0.01 vs. 0.55 ± 0.06, Pl0.01) compared to WT.ConclusionsAlpha1A-AR provides an important counterbalance to pathologic pathways during post-MI remodeling that may be mediated through ERK1/2 signaling; these observations provide support for further development of an alpha1A-AR/ERK-based molecular intervention for this chronic, often fatal disease.
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- 2017
26. Inflammatory and apoptotic remodeling in autonomic nervous system following myocardial infarction
- Author
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Christoph Rau, Kalyanam Shivkumar, Tatsuo Takamiya, Aman Mahajan, Chen Gao, Yibin Wang, Yang Song, Kimberly Howard-Quijano, and Fan, Guo-Chang
- Subjects
Male ,0301 basic medicine ,Nervous system ,Pathology ,Swine ,Stellate Ganglion ,Myocardial Infarction ,lcsh:Medicine ,Gene Expression ,Apoptosis ,030204 cardiovascular system & hematology ,Cardiovascular ,Regenerative Medicine ,Pathology and Laboratory Medicine ,Vascular Medicine ,0302 clinical medicine ,Ischemia ,Ganglia, Spinal ,Medicine and Health Sciences ,2.1 Biological and endogenous factors ,Myocardial infarction ,Aetiology ,lcsh:Science ,Immune Response ,Multidisciplinary ,Cell Death ,Genomics ,Heart Disease ,medicine.anatomical_structure ,Cell Processes ,Cardiology ,Anatomy ,medicine.symptom ,Transcriptome Analysis ,Arrhythmia ,Biotechnology ,Research Article ,medicine.medical_specialty ,Spinal ,General Science & Technology ,Immunology ,Inflammation ,03 medical and health sciences ,Signs and Symptoms ,Diagnostic Medicine ,Internal medicine ,Genetics ,medicine ,Animals ,Heart Disease - Coronary Heart Disease ,business.industry ,Gene Expression Profiling ,lcsh:R ,Neurosciences ,Biology and Life Sciences ,Computational Biology ,Cardiac arrhythmia ,Cell Biology ,Genome Analysis ,medicine.disease ,Gene expression profiling ,Autonomic nervous system ,Good Health and Well Being ,Biological Tissue ,030104 developmental biology ,Myocardial infarction complications ,lcsh:Q ,Ganglia ,business - Abstract
Author(s): Gao, Chen; Howard-Quijano, Kimberly; Rau, Christoph; Takamiya, Tatsuo; Song, Yang; Shivkumar, Kalyanam; Wang, Yibin; Mahajan, Aman | Abstract: BackgroundChronic myocardial infarction (MI) triggers pathological remodeling in the heart and cardiac nervous system. Abnormal function of the autonomic nervous system (ANS), including stellate ganglia (SG) and dorsal root ganglia (DRG) contribute to increased sympathoexcitation, cardiac dysfunction and arrythmogenesis. ANS modulation is a therapeutic target for arrhythmia associated with cardiac injury. However, the molecular mechanism involved in the pathological remodeling in ANS following cardiac injury remains to be established.Methods and resultsIn this study, we performed transcriptome analysis by RNA-sequencing in thoracic SG and (T1-T4) DRG obtained from Yorkshire pigs following either acute (3 to 5 hours) or chronic (8 weeks) myocardial infarction. By differential expression and weighted gene co-expression network analysis (WGCNA), we identified significant transcriptome changes and specific gene modules in the ANS tissues in response to myocardial infarction at either acute or chronic phases. Both differential expressed genes and the member genes of the WGCNA gene module associated with post-infarct condition were significantly enriched for inflammatory signaling and apoptotic cell death. Targeted validation analysis supported a significant induction of inflammatory and apoptotic signal in both SG and DRG following myocardial infarction, along with cellular evidence of apoptosis induction based on TUNEL analysis. Importantly, these molecular changes were observed specifically in the thoracic segments but not in their counterparts obtained from lumbar sections.ConclusionMyocardial injury leads to time-dependent global changes in gene expression in the innervating ANS. Induction of inflammatory gene expression and loss of neuron cell viability in SG and DRG are potential novel mechanisms contributing to abnormal ANS function which can promote cardiac arrhythmia and pathological remodeling in myocardium.
- Published
- 2017
27. In Vivo Cannulation Methods for Cardiomyocytes Isolation from Heart Disease Models
- Author
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Robert S. Ross, Ye Chen-Izu, Yi-Je Chen, Zhong Jian, Nipavan Chiamvimonvat, Mark Jaradeh, Jil C. Tardiff, Karen S. Chavez, Rafael Shimkunas, Yuwen Jian, Leighton T. Izu, and Fan, Guo-Chang
- Subjects
Male ,0301 basic medicine ,Cardiac Catheterization ,Pathology ,Muscle Physiology ,Heart disease ,Physiology ,medicine.medical_treatment ,lcsh:Medicine ,Action Potentials ,Cell Separation ,Cardiovascular Medicine ,030204 cardiovascular system & hematology ,Cardiovascular ,Inbred C57BL ,Transgenic ,Mice ,0302 clinical medicine ,Animal Cells ,Medicine and Health Sciences ,Myocyte ,Myocytes, Cardiac ,lcsh:Science ,Aorta ,Cardiac catheterization ,Multidisciplinary ,Heart ,Arteries ,Adrenergic beta-Agonists ,Heart Disease ,Carotid Arteries ,Cardiovascular Diseases ,Cardiology ,Digestion ,Anatomy ,Cellular Types ,Cardiac ,Research Article ,Muscle Contraction ,Agonist ,medicine.medical_specialty ,General Science & Technology ,Imaging Techniques ,medicine.drug_class ,Muscle Tissue ,Ischemia ,Mice, Transgenic ,Research and Analysis Methods ,03 medical and health sciences ,In vivo ,medicine.artery ,Internal medicine ,Fluorescence Imaging ,medicine ,Animals ,Calcium Signaling ,Heart Disease - Coronary Heart Disease ,Myocytes ,Muscle Cells ,business.industry ,lcsh:R ,Isoproterenol ,Biology and Life Sciences ,Cell Biology ,medicine.disease ,Myocardial Contraction ,In vitro ,Mice, Inbred C57BL ,Biological Tissue ,030104 developmental biology ,Cardiovascular Anatomy ,Blood Vessels ,lcsh:Q ,Physiological Processes ,business - Abstract
Isolation of high quality cardiomyocytes is critically important for achieving successful experiments in many cellular and molecular cardiology studies. Methods for isolating cardiomyocytes from the murine heart generally are time-sensitive and experience-dependent, and often fail to produce high quality cells. Major technical difficulties can be related to the surgical procedures needed to explant the heart and to cannulate the vessel to mount onto the Langendorff system before in vitro reperfusion can begin. During this period, transient hypoxia and ischemia may damage the heart, resulting in low yield and poor quality of cells, especially for heart disease models that have fragile cells. We have developed novel in vivo cannulation methods to minimize hypoxia and ischemia, and fine-tuned the entire protocol to produce high quality ventricular myocytes. The high cell quality has been confirmed using important structural and functional criteria such as morphology, t-tubule structure, action potential morphology, Ca2+ signaling, responsiveness to beta-adrenergic agonist, and ability to have robust contraction under mechanically loaded condition. Together these assessments show the preservation of the cardiac excitation-contraction machinery in cells isolated using this technique. The in vivo cannulation method enables consistent isolation of high-quality cardiomyocytes, even from heart disease models that were notoriously difficult for cell isolation using traditional methods.
- Published
- 2016
28. Toll-like receptor (TLR) 2 and TLR4 differentially regulate doxorubicin induced cardiomyopathy in mice.
- Author
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Ma Y, Zhang X, Bao H, Mi S, Cai W, Yan H, Wang Q, Wang Z, Yan J, Fan GC, Lindsey ML, and Hu Z
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- Acute Disease, Animals, Antibodies, Neutralizing immunology, Autophagy, Cardiomyopathy, Dilated physiopathology, Cardiomyopathy, Dilated therapy, Chronic Disease, Doxorubicin, Heart Function Tests, Inflammation pathology, Male, Mice, Mice, Inbred C57BL, Mice, Inbred ICR, Models, Biological, Signal Transduction, Survival Analysis, Toll-Like Receptor 2 immunology, Cardiomyopathy, Dilated immunology, Cardiomyopathy, Dilated pathology, Toll-Like Receptor 2 metabolism, Toll-Like Receptor 4 metabolism
- Abstract
Recent evidence indicates that toll-like receptor (TLR) 2 and 4 are involved in the pathogenesis of dilated cardiomyopathy (DCM), but the exact mechanisms of their actions have not been elucidated. We explored the therapeutic potential of blocking TLRs in mice with established cardiomyopathy. Cardiomyopathy was generated by a single intraperitoneal injection of doxorubicin (10 mg/kg). Two weeks later, the mice were treated with TLR2 or TLR4 neutralizing antibody. Blocking TLR2, but not TLR4, activity not only reduced mortality, but also attenuated doxorubicin-induced cardiac dysfunction by 20% and inhibited myocardial fibrosis. To determine the differential effects of blocking TLR2 and TLR4 in chronic cardiomyopathy, mice were injected with doxorubicin (3.5 mg/kg) once a week for 8 weeks, followed by treatment with TLR2 or TLR4 neutralizing antibody for 40 days. Blocking TLR2 activity blunted cardiac dysfunction by 13% and inhibited cardiac fibrosis, which was associated with a significant suppression of myocardial inflammation. The underlying mechanism involved interrupting the interaction of TLR2 with its endogenous ligands, resulting in attenuation of inflammation and fibrosis. In contrast, blocking TLR4 exacerbated cardiac dysfunction and fibrosis by amplifying inflammation and suppressing autophagy. Our studies demonstrate that TLR2 and TLR4 play distinct roles in the progression of doxorubicin-induced DCM. TLR4 activity is crucial for the resolution of inflammation and cardiac fibrosis, while blocking TLR2 activity has therapeutic potential for the treatment of DCM.
- Published
- 2012
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