Full metadata record
DC Field | Value | Language |
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dc.contributor.author | 강덕희 | - |
dc.date.accessioned | 2018-05-02T08:15:27Z | - |
dc.date.available | 2018-05-02T08:15:27Z | - |
dc.date.issued | 2004 | - |
dc.identifier.issn | 0363-6127 | - |
dc.identifier.other | OAK-2337 | - |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/242700 | - |
dc.description.abstract | VEGF expression by proximal tubular epithelial cells may play a critical role in maintaining peritubular capillary endothelium in renal disease. Two major processes involved in renal injury include hypoxia (from vasoconstriction or vascular injury) and transforming growth factor (TGF)-β-dependent fibrosis, both of which are known to stimulate VEGF. Because the TGF-β/Smad pathway is activated in hypoxia, we tested the hypothesis that the induction of VEGF in hypoxia could be partially dependent on TGF-β. Rat proximal tubular (NRK52E) cells treated with TGF-β under normoxic conditions secreted VEGF at 24 h, and this was significantly reduced by blocking Smad activation by overexpressing the inhibitory Smad7 or by blocking p38 and ERK1/2 MAP kinase activation or protein kinase C activation with specific inhibitors. With acute hypoxia, rat proximal tubular cells also express VEGF mRNA and protein as well as TGF-β. However, the induction of VEGF occurs before synthesis of TGF-β and is not blocked by either a TGF-β antagonist, by Smad7 overexpression, or by blockage of ERK1/2, whereas induction is blocked by PKC inhibition or partially blocked by a p38 inhibitor. Finally, the addition of TGF-β with hypoxia results in significantly more VEGF expression than either stimulation alone. Thus TGF-β and hypoxia act via additive/synergistic but distinct pathways to stimulate VEGF in proximal tubular cells, a finding that may be important in understanding how VEGF is stimulated in renal disease. | - |
dc.language | English | - |
dc.title | Differential regulation of VEGF by TGF-β and hypoxia in rat proximal tubular cells | - |
dc.type | Article | - |
dc.relation.issue | 4 56-4 | - |
dc.relation.volume | 287 | - |
dc.relation.index | SCOPUS | - |
dc.relation.startpage | F658 | - |
dc.relation.lastpage | F664 | - |
dc.relation.journaltitle | American Journal of Physiology - Renal Physiology | - |
dc.identifier.doi | 10.1152/ajprenal.00040.2004 | - |
dc.identifier.wosid | WOS:000223664300008 | - |
dc.identifier.scopusid | 2-s2.0-4644298996 | - |
dc.author.google | Nakagawa T. | - |
dc.author.google | Lan H.Y. | - |
dc.author.google | Zhu H.J. | - |
dc.author.google | Kang D.-H. | - |
dc.author.google | Schreiner G.F. | - |
dc.author.google | Johnson R.J. | - |
dc.contributor.scopusid | 강덕희(17233695600) | - |
dc.date.modifydate | 20230210140157 | - |