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Signal transducer and activator of transcription 3 is required for glycoprotein 130-mediated induction of vascular endothelial growth factor in cardiac myocytes 总被引:11,自引:0,他引:11
Funamoto M Fujio Y Kunisada K Negoro S Tone E Osugi T Hirota H Izumi M Yoshizaki K Walsh K Kishimoto T Yamauchi-Takihara K 《The Journal of biological chemistry》2000,275(14):10561-10566
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Regulation of vascular endothelial growth factor expression by advanced glycation end products 总被引:40,自引:0,他引:40
Treins C Giorgetti-Peraldi S Murdaca J Van Obberghen E 《The Journal of biological chemistry》2001,276(47):43836-43841
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K Maemura C M Hsieh M K Jain S Fukumoto M D Layne Y Liu S Kourembanas S F Yet M A Perrella M E Lee 《The Journal of biological chemistry》1999,274(44):31565-31570
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Induction of hypoxia-inducible factor-1alpha by transcriptional and translational mechanisms 总被引:15,自引:0,他引:15
Pagé EL Robitaille GA Pouysségur J Richard DE 《The Journal of biological chemistry》2002,277(50):48403-48409
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Induction of vascular endothelial growth factor expression and hypoxia-inducible factor 1alpha protein by the oxidative stressor arsenite 总被引:4,自引:0,他引:4
Duyndam MC Hulscher TM Fontijn D Pinedo HM Boven E 《The Journal of biological chemistry》2001,276(51):48066-48076
Recent evidence suggests that vascular endothelial growth factor (VEGF) expression is up-regulated by oxidative stressors through activation of hypoxia-inducible Factor 1 (HIF-1). To investigate whether this is a general phenomenon, we studied the effects of the sulfhydryl reagent arsenite on VEGF expression in human ovarian cancer cells. Arsenite potently induces the production of reactive oxygen species (ROS) in several cell systems and directly interacts with sulfhydryl groups of cellular thiols. We report that arsenite induces VEGF mRNA and protein levels in normoxic H134 and OVCAR-3 cells. Arsenite also increases HIF-1alpha protein levels, suggesting a role for HIF-1 in the induction of VEGF expression. Pretreatment with the ROS inhibitors catalase and mannitol attenuated arsenite-induced ROS production, but did not affect induction of VEGF mRNA and HIF-1alpha protein. In contrast, pretreatment with the thiol antioxidants glutathione or N-acetylcysteine completely abrogated both effects, whereas a potentiation was observed by depletion of intracellular glutathione. These results demonstrate that arsenite-induced VEGF mRNA and HIF-1alpha protein expression is independent of increased ROS production but critically regulated by the cellular reduced glutathione content. In addition, these data suggest the involvement of a thiol-sensitive mechanism in the regulation of VEGF mRNA expression and HIF-1alpha protein in human ovarian cancer cells. 相似文献
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Hossain MA Bouton CM Pevsner J Laterra J 《The Journal of biological chemistry》2000,275(36):27874-27882
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Gao N Ding M Zheng JZ Zhang Z Leonard SS Liu KJ Shi X Jiang BH 《The Journal of biological chemistry》2002,277(35):31963-31971
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Duyndam MC Hulscher ST van der Wall E Pinedo HM Boven E 《The Journal of biological chemistry》2003,278(9):6885-6895
Recently we have demonstrated that sodium arsenite induces the expression of hypoxia-inducible factor 1alpha (HIF-1alpha) protein and vascular endothelial growth factor (VEGF) in OVCAR-3 human ovarian cancer cells. We now show that arsenic trioxide, an experimental anticancer drug, exerts the same effects. The involvement of phosphatidylinositol 3-kinase and mitogen-activated protein kinase (MAPK) pathways in the effects of sodium arsenite was investigated. By using kinase inhibitors in OVCAR-3 cells, both effects of sodium arsenite were found to be independent of phosphatidylinositol 3-kinase and p44/p42 MAPKS but were attenuated by inhibition of p38 MAPK. A role for p38 in the regulation of HIF-1alpha and VEGF expression was supported further by analysis of activation kinetics. Experiments in mouse fibroblast cell lines, lacking expression of c-Jun N-terminal kinases 1 and 2, suggested that these kinases are not required for induction of HIF-1alpha protein and VEGF mRNA. Unexpectedly, sodium arsenite did not activate a HIF-1-dependent reporter gene in OVCAR-3 cells, indicating that functional HIF-1 was not induced. In agreement with this hypothesis, up-regulation of VEGF mRNA was not reduced in HIF-1alpha(-/-) mouse fibroblast cell lines. Altogether, these data suggest that not HIF-1, but rather p38, mediates induction of VEGF mRNA expression by sodium arsenite. 相似文献
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HER2 (neu) signaling increases the rate of hypoxia-inducible factor 1alpha (HIF-1alpha) synthesis: novel mechanism for HIF-1-mediated vascular endothelial growth factor expression 总被引:8,自引:0,他引:8
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Laughner E Taghavi P Chiles K Mahon PC Semenza GL 《Molecular and cellular biology》2001,21(12):3995-4004
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