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10.1038/cddis.2013.551 http://scihub22266oqcxt.onion/10.1038/cddis.2013.551 C4040700!4040700!24457954     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Death+Dis 2014 ; 5 (1): e1010- Nephropedia Template TP {{tp|p=24457954|t=2014. Nox4 and redox signaling mediate TGF-?-induced endothelial cell apoptosis and phenotypic switch |pdf=|usr=}}{{24457954}} gab.com Text Nox4 and redox signaling mediate TGF- -induced endothelial cell apoptosis and phenotypic switch JO: Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=24457954 #FOAvip Transforming growth factor-? (TGF-?) triggers apoptosis in endothelial cells, while the mechanisms underlying this action are not entirely understood. Using genetic and pharmacological tools, we demonstrated that TGF-? induced a moderate apoptotic response in human cultured endothelial cells, which was dependent upon upregulation of the Nox4 NADPH oxidase and production of reactive oxygen species (ROS). In contrast, we showed that ectopic expression of Nox4 via viral vectors (vNox4) produced an antiapoptotic effect. TGF-? caused ROS-dependent p38 activation, whereas inhibition of p38 blunted TGF-?-induced apoptosis. However, vNox4, but not TGF-?, activated Akt, and inhibition of Akt attenuated the antiapoptotic effect of vNox4. Akt activation induced by vNox4 was accompanied by inactivation of the protein tyrosine phosphatase-1B (PTP1B) function and enhanced vascular endothelial growth factor receptor (VEGFR)-2 phosphorylation. Moreover, we showed that TGF-? enhanced Notch signaling and increased expression of the arterial marker EphrinB2 in a redox-dependent manner. In summary, our results suggest that Nox4 and ROS have pivotal roles in mediating TGF-?-induced endothelial apoptosis and phenotype specification. Redox mechanisms may influence endothelial cell functions by modulating p38, PTP1B/VEGFR/Akt and Notch signaling pathways. Twit Text FOAVip Nox4 and redox signaling mediate TGF- -induced endothelial cell apoptosis and phenotypic switch ????Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=24457954 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24457954 #FOAvip English Wikipedia <ref>{{Cite pmid|24457954}}</ref> Nox4 and redox signaling mediate TGF-?-induced endothelial cell apoptosis and phenotypic switch #MMPMID24457954 Yan F; Wang Y; Wu X; Peshavariya HM; Dusting GJ; Zhang M; Jiang F Cell Death Dis 2014[Jan]; 5 (1): e1010- PMID24457954show ga Transforming growth factor-? (TGF-?) triggers apoptosis in endothelial cells, while the mechanisms underlying this action are not entirely understood. Using genetic and pharmacological tools, we demonstrated that TGF-? induced a moderate apoptotic response in human cultured endothelial cells, which was dependent upon upregulation of the Nox4 NADPH oxidase and production of reactive oxygen species (ROS). In contrast, we showed that ectopic expression of Nox4 via viral vectors (vNox4) produced an antiapoptotic effect. TGF-? caused ROS-dependent p38 activation, whereas inhibition of p38 blunted TGF-?-induced apoptosis. However, vNox4, but not TGF-?, activated Akt, and inhibition of Akt attenuated the antiapoptotic effect of vNox4. Akt activation induced by vNox4 was accompanied by inactivation of the protein tyrosine phosphatase-1B (PTP1B) function and enhanced vascular endothelial growth factor receptor (VEGFR)-2 phosphorylation. Moreover, we showed that TGF-? enhanced Notch signaling and increased expression of the arterial marker EphrinB2 in a redox-dependent manner. In summary, our results suggest that Nox4 and ROS have pivotal roles in mediating TGF-?-induced endothelial apoptosis and phenotype specification. Redox mechanisms may influence endothelial cell functions by modulating p38, PTP1B/VEGFR/Akt and Notch signaling pathways. äNox4 and redox signaling mediate TGF-?-induced endothelial cell apopto(epmc).pdf DeepDyve Pubget Overpricing