12 results on '"Jianxin, Sun"'
Search Results
2. Correction: MicroRNA-138 Regulates Hypoxia-Induced Endothelial Cell Dysfunction By Targeting S100A1.
- Author
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Anagha Sen, Shumei Ren, Carolin Lerchenmüller, Jianxin Sun, Norbert Weiss, Patrick Most, and Karsten Peppel
- Subjects
Medicine ,Science - Published
- 2013
- Full Text
- View/download PDF
3. Glyceraldehyde-3-phosphate dehydrogenase interacts with proapoptotic kinase mst1 to promote cardiomyocyte apoptosis.
- Author
-
Bei You, Shengdong Huang, Qing Qin, Bing Yi, Yang Yuan, Zhiyun Xu, and Jianxin Sun
- Subjects
Medicine ,Science - Abstract
Mammalian sterile 20-like kinase 1 (Mst1) is a critical component of the Hippo signaling pathway, which regulates a variety of biological processes ranging from cell contact inhibition, organ size control, apoptosis and tumor suppression in mammals. Mst1 plays essential roles in the heart disease since its activation causes cardiomyocyte apoptosis and dilated cardiomyopathy. However, the mechanism underlying Mst1 activation in the heart remains unknown. In a yeast two-hybrid screen of a human heart cDNA library with Mst1 as bait, glyceraldehyde-3-phosphate dehydrogenase (GAPDH) was identified as an Mst1-interacting protein. The interaction of GAPDH with Mst1 was confirmed by co-immunoprecipitation in both co-transfected HEK293 cells and mouse heart homogenates, in which GAPDH interacted with the kinase domain of Mst1, whereas the C-terminal catalytic domain of GAPDH mediated its interaction with Mst1. Moreover, interaction of Mst1 with GAPDH caused a robust phosphorylation of GAPDH and markedly increased the Mst1 activity in cells. Chelerythrine, a potent inducer of apoptosis, substantially increased the nuclear translocation and interaction of GAPDH and Mst1 in cardiomyocytes. Overexpression of GAPDH significantly augmented the Mst1 mediated apoptosis, whereas knockdown of GAPDH markedly attenuated the Mst1 activation and cardiomyocyte apoptosis in response to either chelerythrine or hypoxia/reoxygenation. These findings reveal a novel function of GAPDH in Mst1 activation and cardiomyocyte apoptosis and suggest that disruption of GAPDH interaction with Mst1 may prevent apoptosis related heart diseases such as heart failure and ischemic heart disease.
- Published
- 2013
- Full Text
- View/download PDF
4. MicroRNA-138 regulates hypoxia-induced endothelial cell dysfunction by targeting S100A1.
- Author
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Anagha Sen, Shumei Ren, Carolin Lerchenmüller, Jianxin Sun, Norbert Weiss, Patrick Most, and Karsten Peppel
- Subjects
Medicine ,Science - Abstract
The Ca(2+) sensor S100A1 is essential for proper endothelial cell (EC) nitric oxide (NO) synthase (eNOS) activation. S100A1 levels are greatly reduced in primary human microvascular ECs subjected to hypoxia, rendering them dysfunctional. However mechanisms that regulate S100A1 levels in ECs are unknown. Here we show that ECs transfected with a S100A1-3' untranslated region (UTR) luciferase reporter construct display significantly reduced gene expression when subjected to low oxygen levels or chemical hypoxia. Bioinformatic analysis suggested that microRNA -138 (MiR-138) could target the 3'UTR of S100A1. Patients with critical limb ischemia (CLI) or mice subjected to femoral artery resection (FAR) displayed increased MiR-138 levels and decreased S100A1 protein expression. Consistent with this finding, hypoxia greatly increased MiR-138 levels in ECs, but not in skeletal muscle C2C12 myoblasts or differentiated myotubes or primary human vascular smooth muscle cells. Transfection of a MiR-138 mimic into ECs reduced S100A1-3 'UTR reporter gene expression, while transfection of an anti MiR-138 prevented the hypoxia-induced downregulation of the reporter gene. Deletion of the 22 nucleotide putative MiR-138 target site abolished the hypoxia-induced loss of reporter gene expression. Knockdown of Hif1-α mediated by siRNA prevented loss of hypoxia-induced reporter gene expression. Conversely, specific activation of Hif1-α by a selective prolyl-hydroxylase inhibitor (IOX2) reduced reporter gene expression even in the absence of hypoxia. Finally, primary ECs transfected with a MiR-138 mimic displayed reduced tube formation when plated onto Matrigel matrix and expressed less NO when stimulated with VEGF. These effects were reversed by gene transfer of S100A1 using recombinant adenovirus. We conclude that hypoxia-induced MiR-138 is an essential mediator of EC dysfunction via its ability to target the 3'UTR of S100A1.
- Published
- 2013
- Full Text
- View/download PDF
5. Specificity responses of grasshoppers in temperate grasslands to diel asymmetric warming.
- Author
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Tingjuan Wu, Shuguang Hao, Osbert Jianxin Sun, and Le Kang
- Subjects
Medicine ,Science - Abstract
Global warming is characterized by not only an increase in the daily mean temperature, but also a diel asymmetric pattern. However, most of the current studies on climate change have only concerned with the mean values of the warming trend. Although many studies have been conducted concerning the responses of insects to climate change, studies that address the issue of diel asymmetric warming under field conditions are not found in the literature.We conducted a field climate manipulative experiment and investigated developmental and demographic responses to diel asymmetric warming in three grasshopper species (an early-season species Dasyhippus barbipes, a mid-season species Oedaleus asiaticus, and a late-season species Chorthippus fallax). It was found that warming generally advanced the development of eggs and nymphs, but had no apparent impacts on the hatching rate of eggs, the emergence rate of nymphs and the survival and fecundity of adults in all the three species. Nighttime warming was more effective in advancing egg development than the daytime warming. The emergence time of adults was differentially advanced by warming in the three species; it was advanced by 5.64 days in C. fallax, 3.55 days in O. asiaticus, and 1.96 days in D. barbipes. This phenological advancement was associated with increases in the effective GDDs accumulation.Results in this study indicate that the responses of the three grasshopper species to warming are influenced by several factors, including species traits, developmental stage, and the thermal sensitivity of the species. Moreover, species with diapausing eggs are less responsive to changes in temperature regimes, suggesting that development of diapausing eggs is a protective mechanism in early-season grasshopper for avoiding the risk of pre-winter hatching. Our results highlight the need to consider the complex relationships between climate change and specificity responses of invertebrates.
- Published
- 2012
- Full Text
- View/download PDF
6. MicroRNA-145 protects cardiomyocytes against hydrogen peroxide (H₂O₂)-induced apoptosis through targeting the mitochondria apoptotic pathway.
- Author
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Ruotian Li, Guijun Yan, Qiaoling Li, Haixiang Sun, Yali Hu, Jianxin Sun, and Biao Xu
- Subjects
Medicine ,Science - Abstract
MicroRNAs, a class of small and non-encoding RNAs that transcriptionally or post-transcriptionally modulate the expression of their target genes, has been implicated as critical regulatory molecules in many cardiovascular diseases, including ischemia/reperfusion induced cardiac injury. Here, we report microRNA-145, a tumor suppressor miRNA, can protect cardiomyocytes from hydrogen peroxide H₂O₂-induced apoptosis through targeting the mitochondrial pathway. Quantitative real-time PCR (qPCR) demonstrated that the expression of miR-145 in either ischemia/reperfused mice myocardial tissues or H₂O₂-treated neonatal rat ventricle myocytes (NRVMs) was markedly down-regulated. Over-expression of miR-145 significantly inhibited the H₂O₂-induced cellular apoptosis, ROS production, mitochondrial structure disruption as well as the activation of key signaling proteins in mitochondrial apoptotic pathway. These protective effects of miR-145 were abrogated by over-expression of Bnip3, an initiation factor of the mitochondrial apoptotic pathway in cardiomyocytes. Finally, we utilized both luciferase reporter assay and western blot analysis to identify Bnip3 as a direct target of miR-145. Our results suggest miR-145 plays an important role in regulating mitochondrial apoptotic pathway in heart challenged with oxidative stress. MiR-145 may represent a potential therapeutic target for treatment of oxidative stress-associated cardiovascular diseases, such as myocardial ischemia/reperfusion injury.
- Published
- 2012
- Full Text
- View/download PDF
7. Orphan nuclear receptor Nur77 regulates androgen receptor gene expression in mouse ovary.
- Author
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Anyi Dai, Guijun Yan, Qinyuan He, Yue Jiang, Qun Zhang, Ting Fang, Lijun Ding, Jianxin Sun, Haixiang Sun, and Yali Hu
- Subjects
Medicine ,Science - Abstract
The androgen receptor (AR) is a nuclear receptor that is expressed in growing follicles and involved in folliculogenesis and follicle growth. The orphan nuclear receptor, Nur77, also has an important role in steroid signaling and follicle maturation. We hypothesized that AR levels and androgen signaling through AR are regulated by Nur77 in the ovary. In the ovaries of Nur77 knockout mice (n = 5), real-time PCR results showed that the mRNA levels of AR and an androgen signaling target gene, Kitl, were decreased by 35% and 24%, respectively, relative to wild-type mice (n = 5), which suggested transcriptional regulation of AR by Nur77 in vivo. In cultured mouse granulosa cells and a steroidogenic human ovarian granulosa-like tumor cell line, KGN, mRNA and protein expression levels of AR were increased by overexpressing Nur77 but decreased by knocking down endogenous Nur77. Consistent with increased AR expression, chromatin immunoprecipitation showed that Nur77 bound to the NGFI-B response element (NBRE) in the AR promoter sequence. AR promoter activity was stimulated by Nur77 in HEK293T cells and attenuated in Nur77 knockout mouse granulosa cells (luciferase assay). Overexpression of Nur77 enhanced the androgenic induction of Kitl (200 nM; 48h), while knockout of Nur77 attenuated this induction. These results demonstrate that AR is regulated by Nur77 in the ovaries, and they suggest that the participation of Nur77 in androgen signaling may be essential for normal follicular development.
- Published
- 2012
- Full Text
- View/download PDF
8. Specificity responses of grasshoppers in temperate grasslands to diel asymmetric warming
- Author
-
Osbert Jianxin Sun, Tingjuan Wu, Shuguang Hao, and Le Kang
- Subjects
Nymph ,Embryology ,Atmospheric Science ,Time Factors ,Climate Change ,Climate ,Climate change ,lcsh:Medicine ,Grasshoppers ,Biology ,Poaceae ,Global Warming ,Species Specificity ,Global Change Ecology ,Animals ,Grasshopper ,lcsh:Science ,Diel vertical migration ,Ovum ,Invertebrate ,Climatology ,Multidisciplinary ,Ecology ,Phenology ,Hatching ,Global warming ,lcsh:R ,Environment, Controlled ,Fecundity ,biology.organism_classification ,Fertility ,Earth Sciences ,Female ,lcsh:Q ,Seasons ,Organism Development ,Zoology ,Entomology ,Research Article ,Developmental Biology - Abstract
Background Global warming is characterized by not only an increase in the daily mean temperature, but also a diel asymmetric pattern. However, most of the current studies on climate change have only concerned with the mean values of the warming trend. Although many studies have been conducted concerning the responses of insects to climate change, studies that address the issue of diel asymmetric warming under field conditions are not found in the literature. Methodology/Principal Findings We conducted a field climate manipulative experiment and investigated developmental and demographic responses to diel asymmetric warming in three grasshopper species (an early-season species Dasyhippus barbipes, a mid-season species Oedaleus asiaticus, and a late-season species Chorthippus fallax). It was found that warming generally advanced the development of eggs and nymphs, but had no apparent impacts on the hatching rate of eggs, the emergence rate of nymphs and the survival and fecundity of adults in all the three species. Nighttime warming was more effective in advancing egg development than the daytime warming. The emergence time of adults was differentially advanced by warming in the three species; it was advanced by 5.64 days in C. fallax, 3.55 days in O. asiaticus, and 1.96 days in D. barbipes. This phenological advancement was associated with increases in the effective GDDs accumulation. Conclusions/Significance Results in this study indicate that the responses of the three grasshopper species to warming are influenced by several factors, including species traits, developmental stage, and the thermal sensitivity of the species. Moreover, species with diapausing eggs are less responsive to changes in temperature regimes, suggesting that development of diapausing eggs is a protective mechanism in early-season grasshopper for avoiding the risk of pre-winter hatching. Our results highlight the need to consider the complex relationships between climate change and specificity responses of invertebrates.
- Published
- 2012
9. Orphan nuclear receptor Nur77 regulates androgen receptor gene expression in mouse ovary
- Author
-
Ting Fang, Yali Hu, Anyi Dai, Lijun Ding, Jianxin Sun, Haixiang Sun, Guijun Yan, Qin-Yuan He, Qun Zhang, and Yue Jiang
- Subjects
Embryology ,Mouse ,Gene Expression ,lcsh:Medicine ,Cell Fate Determination ,Mice ,Molecular Cell Biology ,Nuclear Receptor Subfamily 4, Group A, Member 1 ,Promoter Regions, Genetic ,lcsh:Science ,Multidisciplinary ,Cell Differentiation ,Animal Models ,Somatic Cells ,Receptors, Androgen ,Knockout mouse ,Female ,Folliculogenesis ,Cellular Types ,Signal transduction ,Research Article ,Signal Transduction ,Chromatin Immunoprecipitation ,Nerve growth factor IB ,medicine.drug_class ,Granulosa cell ,Blotting, Western ,Biology ,Real-Time Polymerase Chain Reaction ,Cell Growth ,Model Organisms ,Genetics ,medicine ,Animals ,Humans ,RNA, Messenger ,Ovary ,lcsh:R ,Androgen ,Molecular biology ,Androgen receptor ,HEK293 Cells ,Germ Cells ,Gene Expression Regulation ,Nuclear receptor ,Fertilization ,lcsh:Q ,Gene Function ,Developmental Biology - Abstract
The androgen receptor (AR) is a nuclear receptor that is expressed in growing follicles and involved in folliculogenesis and follicle growth. The orphan nuclear receptor, Nur77, also has an important role in steroid signaling and follicle maturation. We hypothesized that AR levels and androgen signaling through AR are regulated by Nur77 in the ovary. In the ovaries of Nur77 knockout mice (n = 5), real-time PCR results showed that the mRNA levels of AR and an androgen signaling target gene, Kitl, were decreased by 35% and 24%, respectively, relative to wild-type mice (n = 5), which suggested transcriptional regulation of AR by Nur77 in vivo. In cultured mouse granulosa cells and a steroidogenic human ovarian granulosa-like tumor cell line, KGN, mRNA and protein expression levels of AR were increased by overexpressing Nur77 but decreased by knocking down endogenous Nur77. Consistent with increased AR expression, chromatin immunoprecipitation showed that Nur77 bound to the NGFI-B response element (NBRE) in the AR promoter sequence. AR promoter activity was stimulated by Nur77 in HEK293T cells and attenuated in Nur77 knockout mouse granulosa cells (luciferase assay). Overexpression of Nur77 enhanced the androgenic induction of Kitl (200 nM; 48h), while knockout of Nur77 attenuated this induction. These results demonstrate that AR is regulated by Nur77 in the ovaries, and they suggest that the participation of Nur77 in androgen signaling may be essential for normal follicular development.
- Published
- 2012
10. Glyceraldehyde-3-Phosphate Dehydrogenase Interacts with Proapoptotic Kinase Mst1 to Promote Cardiomyocyte Apoptosis
- Author
-
Bing Yi, Bei You, Yang Yuan, Zhi-yun Xu, Jianxin Sun, Shengdong Huang, and Qing Qin
- Subjects
Proteomics ,MST1 ,lcsh:Medicine ,Apoptosis ,Cardiovascular ,Biochemistry ,Mice ,chemistry.chemical_compound ,0302 clinical medicine ,Molecular Cell Biology ,Signaling in Cellular Processes ,Myocytes, Cardiac ,lcsh:Science ,Apoptotic Signaling Cascade ,Glyceraldehyde 3-phosphate dehydrogenase ,Apoptotic Signaling ,Cellular Stress Responses ,0303 health sciences ,Multidisciplinary ,Cell Death ,Hepatocyte Growth Factor ,Kinase ,Intracellular Signaling Peptides and Proteins ,Glyceraldehyde-3-Phosphate Dehydrogenases ,Signaling Cascades ,Cell biology ,Gene Knockdown Techniques ,030220 oncology & carcinogenesis ,Medicine ,Phosphorylation ,Cardiomyopathies ,Research Article ,Signal Transduction ,Protein Serine-Threonine Kinases ,Biology ,Cell Line ,03 medical and health sciences ,stomatognathic system ,Proto-Oncogene Proteins ,Two-Hybrid System Techniques ,Animals ,Humans ,Protein Interaction Domains and Motifs ,Protein Interactions ,030304 developmental biology ,Hippo signaling pathway ,lcsh:R ,Proteins ,Molecular biology ,Rats ,Mice, Inbred C57BL ,HEK293 Cells ,Chelerythrine ,chemistry ,Protein kinase domain ,biology.protein ,lcsh:Q - Abstract
Mammalian sterile 20-like kinase 1 (Mst1) is a critical component of the Hippo signaling pathway, which regulates a variety of biological processes ranging from cell contact inhibition, organ size control, apoptosis and tumor suppression in mammals. Mst1 plays essential roles in the heart disease since its activation causes cardiomyocyte apoptosis and dilated cardiomyopathy. However, the mechanism underlying Mst1 activation in the heart remains unknown. In a yeast two-hybrid screen of a human heart cDNA library with Mst1 as bait, glyceraldehyde-3-phosphate dehydrogenase (GAPDH) was identified as an Mst1-interacting protein. The interaction of GAPDH with Mst1 was confirmed by co-immunoprecipitation in both co-transfected HEK293 cells and mouse heart homogenates, in which GAPDH interacted with the kinase domain of Mst1, whereas the C-terminal catalytic domain of GAPDH mediated its interaction with Mst1. Moreover, interaction of Mst1 with GAPDH caused a robust phosphorylation of GAPDH and markedly increased the Mst1 activity in cells. Chelerythrine, a potent inducer of apoptosis, substantially increased the nuclear translocation and interaction of GAPDH and Mst1 in cardiomyocytes. Overexpression of GAPDH significantly augmented the Mst1 mediated apoptosis, whereas knockdown of GAPDH markedly attenuated the Mst1 activation and cardiomyocyte apoptosis in response to either chelerythrine or hypoxia/reoxygenation. These findings reveal a novel function of GAPDH in Mst1 activation and cardiomyocyte apoptosis and suggest that disruption of GAPDH interaction with Mst1 may prevent apoptosis related heart diseases such as heart failure and ischemic heart disease.
- Published
- 2013
11. MicroRNA-145 Protects Cardiomyocytes against Hydrogen Peroxide (H2O2)-Induced Apoptosis through Targeting the Mitochondria Apoptotic Pathway
- Author
-
Yali Hu, Haixiang Sun, Biao Xu, Guijun Yan, Jianxin Sun, Ruotian Li, and Qiaoling Li
- Subjects
chemistry.chemical_classification ,0303 health sciences ,Reactive oxygen species ,Multidisciplinary ,medicine.diagnostic_test ,Oxidative phosphorylation ,Mitochondrion ,Biology ,medicine.disease_cause ,medicine.disease ,Molecular biology ,3. Good health ,Cell biology ,03 medical and health sciences ,0302 clinical medicine ,chemistry ,Western blot ,Apoptosis ,030220 oncology & carcinogenesis ,microRNA ,medicine ,Reperfusion injury ,Oxidative stress ,030304 developmental biology - Abstract
MicroRNAs, a class of small and non-encoding RNAs that transcriptionally or post-transcriptionally modulate the expression of their target genes, has been implicated as critical regulatory molecules in many cardiovascular diseases, including ischemia/reperfusion induced cardiac injury. Here, we report microRNA-145, a tumor suppressor miRNA, can protect cardiomyocytes from hydrogen peroxide (H2O2)-induced apoptosis through targeting the mitochondrial pathway. Quantitative real-time PCR (qPCR) demonstrated that the expression of miR-145 in either ischemia/reperfused mice myocardial tissues or H2O2-treated neonatal rat ventricle myocytes (NRVMs) was markedly down-regulated. Over-expression of miR-145 significantly inhibited the H2O2-induced cellular apoptosis, ROS production, mitochondrial structure disruption as well as the activation of key signaling proteins in mitochondrial apoptotic pathway. These protective effects of miR-145 were abrogated by over-expression of Bnip3, an initiation factor of the mitochondrial apoptotic pathway in cardiomyocytes. Finally, we utilized both luciferase reporter assay and western blot analysis to identify Bnip3 as a direct target of miR-145. Our results suggest miR-145 plays an important role in regulating mitochondrial apoptotic pathway in heart challenged with oxidative stress. MiR-145 may represent a potential therapeutic target for treatment of oxidative stress-associated cardiovascular diseases, such as myocardial ischemia/reperfusion injury.
- Published
- 2012
12. MicroRNA-145 Protects Cardiomyocytes against Hydrogen Peroxide (H2O2)-Induced Apoptosis through Targeting the Mitochondria Apoptotic Pathway.
- Author
-
Ruotian Li, Guijun Yan, Qiaoling Li, Haixiang Sun, Yali Hu, Jianxin Sun, Biao Xu, and Kukreja, Rakesh
- Subjects
MICRORNA ,HYDROGEN peroxide ,MITOCHONDRIA ,APOPTOSIS ,HEART cells ,OXIDATIVE stress - Abstract
MicroRNAs, a class of small and non-encoding RNAs that transcriptionally or post-transcriptionally modulate the expression of their target genes, has been implicated as critical regulatory molecules in many cardiovascular diseases, including ischemia/reperfusion induced cardiac injury. Here, we report microRNA-145, a tumor suppressor miRNA, can protect cardiomyocytes from hydrogen peroxide (H
2 O2 )-induced apoptosis through targeting the mitochondrial pathway. Quantitative real-time PCR (qPCR) demonstrated that the expression of miR-145 in either ischemia/reperfused mice myocardial tissues or H2 O2 -treated neonatal rat ventricle myocytes (NRVMs) was markedly down-regulated. Over-expression of miR-145 significantly inhibited the H H2 O2 -induced cellular apoptosis, ROS production, mitochondrial structure disruption as well as the activation of key signaling proteins in mitochondrial apoptotic pathway. These protective effects of miR-145 were abrogated by over-expression of Bnip3, an initiation factor of the mitochondrial apoptotic pathway in cardiomyocytes. Finally, we utilized both luciferase reporter assay and western blot analysis to identify Bnip3 as a direct target of miR-145. Our results suggest miR-145 plays an important role in regulating mitochondrial apoptotic pathway in heart challenged with oxidative stress. MiR-145 may represent a potential therapeutic target for treatment of oxidative stress-associated cardiovascular diseases, such as myocardial ischemia/reperfusion injury. [ABSTRACT FROM AUTHOR]- Published
- 2012
- Full Text
- View/download PDF
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