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10.1159/000444719 http://scihub22266oqcxt.onion/10.1159/000444719 C4828273!4828273!26930122     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\26930122.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Am+J+Nephrol 2016 ; 43 (2): 74-84 Nephropedia Template TP {{tp|p=26930122|t=2016. VEGF AND PODOCYTE PROTECTION IN CHRONIC HYPOXIA: EFFECTS OF ENDOTHELIN-A RECEPTOR ANTAGONISM |pdf=|usr=}}{{26930122}} gab.com Text VEGF AND PODOCYTE PROTECTION IN CHRONIC HYPOXIA: EFFECTS OF ENDOTHELIN-A RECEPTOR ANTAGONISM JO: Am J Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=26930122 #FOAvip Background: Podocytes are major components of the filtration barrier and a renal source of vascular endothelial growth factor (VEGF). Chronic renovascular disease (RVD) progressively deteriorates renal function, accompanied by podocyte damage and a progressive reduction in VEGF. We showed that the endothelin (ET) pathway contributes to this pathological process and ET-A (but not ET-B) receptor antagonism protects the kidney in RVD. We hypothesize that ETA-induced renoprotection is largely driven by protection of podocyte integrity and function. Methods: To mimic renal environment of chronic RVD, human podocytes were incubated under chronic hypoxia for 96 hours and divided in untreated or treated with an ET-A or ET-B receptor antagonist. Cells were quantified after 96 hours. Cell homogenates and media were obtained after 1, 24 and 96 hours to quantify production of VEGF, anti-VEGF soluble receptor s-Flt1, and the expression of apoptotic mediators. A separate set of similar experiments was performed after addition of a VEGF-neutralizing antibody (VEGF-NA). Results: Hypoxia decreased podocyte number, which was exacerbated by ET-B but improved after ET-A antagonism. Production of VEGF was preserved by ET-A antagonism whereas s-Flt1 increased in hypoxic cells after ET-B antagonism only, accompanied by a greater expression of pro-apoptotic mediators. On the other hand, treatment with VEGF-NA diminished ET-A-induced protection of podocytes. Conclusion: ET-A antagonism preserves podocyte viability and integrity under chronic hypoxia, whereas ET-B antagonism exacerbates podocyte dysfunction and death. Enhanced bioavailability of VEGF after ET-A antagonism could be a pivotal mechanism of podocyte protection that significantly contributes to ET-A receptor blockade-induced renal recovery in chronic RVD. Twit Text FOAVip VEGF AND PODOCYTE PROTECTION IN CHRONIC HYPOXIA: EFFECTS OF ENDOTHELIN-A RECEPTOR ANTAGONISM ????Am J Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=26930122 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26930122 #FOAvip English Wikipedia <ref>{{Cite pmid|26930122}}</ref> VEGF AND PODOCYTE PROTECTION IN CHRONIC HYPOXIA: EFFECTS OF ENDOTHELIN-A RECEPTOR ANTAGONISM #MMPMID26930122 Harvey TW; Engel JE; Chade AR Am J Nephrol 2016[]; 43 (2): 74-84 PMID26930122show ga Background: Podocytes are major components of the filtration barrier and a renal source of vascular endothelial growth factor (VEGF). Chronic renovascular disease (RVD) progressively deteriorates renal function, accompanied by podocyte damage and a progressive reduction in VEGF. We showed that the endothelin (ET) pathway contributes to this pathological process and ET-A (but not ET-B) receptor antagonism protects the kidney in RVD. We hypothesize that ETA-induced renoprotection is largely driven by protection of podocyte integrity and function. Methods: To mimic renal environment of chronic RVD, human podocytes were incubated under chronic hypoxia for 96 hours and divided in untreated or treated with an ET-A or ET-B receptor antagonist. Cells were quantified after 96 hours. Cell homogenates and media were obtained after 1, 24 and 96 hours to quantify production of VEGF, anti-VEGF soluble receptor s-Flt1, and the expression of apoptotic mediators. A separate set of similar experiments was performed after addition of a VEGF-neutralizing antibody (VEGF-NA). Results: Hypoxia decreased podocyte number, which was exacerbated by ET-B but improved after ET-A antagonism. Production of VEGF was preserved by ET-A antagonism whereas s-Flt1 increased in hypoxic cells after ET-B antagonism only, accompanied by a greater expression of pro-apoptotic mediators. On the other hand, treatment with VEGF-NA diminished ET-A-induced protection of podocytes. Conclusion: ET-A antagonism preserves podocyte viability and integrity under chronic hypoxia, whereas ET-B antagonism exacerbates podocyte dysfunction and death. Enhanced bioavailability of VEGF after ET-A antagonism could be a pivotal mechanism of podocyte protection that significantly contributes to ET-A receptor blockade-induced renal recovery in chronic RVD. äVEGF AND PODOCYTE PROTECTION IN CHRONIC HYPOXIA: EFFECTS OF ENDOTHELIN(epmc).pdf DeepDyve Pubget Overpricing