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10.1038/cddis.2014.131 http://scihub22266oqcxt.onion/10.1038/cddis.2014.131 C5424109!5424109!24722289     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 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Death+Dis 2014 ; 5 (4): e1164- Nephropedia Template TP {{tp|p=24722289|t=2014. Selective inhibition of protein kinase C ?2 attenuates the adaptor P66Shc-mediated intestinal ischemia?reperfusion injury |pdf=|usr=}}{{24722289}} gab.com Text Selective inhibition of protein kinase C 2 attenuates the adaptor P66Shc-mediated intestinal ischemia reperfusion injury JO: Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=24722289 #FOAvip Apoptosis is a major mode of cell death occurring during ischemia?reperfusion (I/R) induced injury. The p66Shc adaptor protein, which is mediated by PKC?, has an essential role in apoptosis under oxidative stress. This study aimed to investigate the role of PKC?2/p66Shc pathway in intestinal I/R injury. In vivo, ischemia was induced by superior mesenteric artery occlusion in mice. Ruboxistaurin (PKC? inhibitor) or normal saline was administered before ischemia. Then blood and gut tissues were collected after reperfusion for various measurements. In vitro, Caco-2 cells were challenged with hypoxia?reoxygenation (H/R) to simulate intestinal I/R. Translocation and activation of PKC?2 were markedly induced in the I/R intestine. Ruboxistaurin significantly attenuated gut damage and decreased the serum levels of tumor necrosis factor-? (TNF-?) and interleukin-6 (IL-6). Pharmacological blockade of PKC?2 suppressed p66Shc overexpression and phosphorylation in the I/R intestine. Gene knockdown of PKC?2 via small interfering RNA (siRNA) inhibited H/R-induced p66Shc overexpression and phosphorylation in Caco-2 cells. Phorbol 12-myristate 13-acetate (PMA), which stimulates PKCs, induced p66Shc phosphorylation and this was inhibited by ruboxistaurin and PKC?2 siRNA. Ruboxistaurin attenuated gut oxidative stress after I/R by suppressing the decreased expression of manganese superoxide dismutase (MnSOD), the exhaustion of the glutathione (GSH) system, and the overproduction of malondialdehyde (MDA). As a consequence, ruboxistaurin inhibited intestinal mucosa apoptosis after I/R. Therefore, PKC?2 inhibition protects mice from gut I/R injury by suppressing the adaptor p66Shc-mediated oxidative stress and subsequent apoptosis. This may represent a novel therapeutic approach for the prevention of intestinal I/R injury. Twit Text FOAVip Selective inhibition of protein kinase C 2 attenuates the adaptor P66Shc-mediated intestinal ischemia reperfusion injury ????Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=24722289 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24722289 #FOAvip English Wikipedia <ref>{{Cite pmid|24722289}}</ref> Selective inhibition of protein kinase C ?2 attenuates the adaptor P66Shc-mediated intestinal ischemia?reperfusion injury #MMPMID24722289 Chen Z; Wang G; Zhai X; Hu Y; Gao D; Ma L; Yao J; Tian X Cell Death Dis 2014[Apr]; 5 (4): e1164- PMID24722289show ga Apoptosis is a major mode of cell death occurring during ischemia?reperfusion (I/R) induced injury. The p66Shc adaptor protein, which is mediated by PKC?, has an essential role in apoptosis under oxidative stress. This study aimed to investigate the role of PKC?2/p66Shc pathway in intestinal I/R injury. In vivo, ischemia was induced by superior mesenteric artery occlusion in mice. Ruboxistaurin (PKC? inhibitor) or normal saline was administered before ischemia. Then blood and gut tissues were collected after reperfusion for various measurements. In vitro, Caco-2 cells were challenged with hypoxia?reoxygenation (H/R) to simulate intestinal I/R. Translocation and activation of PKC?2 were markedly induced in the I/R intestine. Ruboxistaurin significantly attenuated gut damage and decreased the serum levels of tumor necrosis factor-? (TNF-?) and interleukin-6 (IL-6). Pharmacological blockade of PKC?2 suppressed p66Shc overexpression and phosphorylation in the I/R intestine. Gene knockdown of PKC?2 via small interfering RNA (siRNA) inhibited H/R-induced p66Shc overexpression and phosphorylation in Caco-2 cells. Phorbol 12-myristate 13-acetate (PMA), which stimulates PKCs, induced p66Shc phosphorylation and this was inhibited by ruboxistaurin and PKC?2 siRNA. Ruboxistaurin attenuated gut oxidative stress after I/R by suppressing the decreased expression of manganese superoxide dismutase (MnSOD), the exhaustion of the glutathione (GSH) system, and the overproduction of malondialdehyde (MDA). As a consequence, ruboxistaurin inhibited intestinal mucosa apoptosis after I/R. Therefore, PKC?2 inhibition protects mice from gut I/R injury by suppressing the adaptor p66Shc-mediated oxidative stress and subsequent apoptosis. This may represent a novel therapeutic approach for the prevention of intestinal I/R injury. äSelective inhibition of protein kinase C ?2 attenuates the adaptor P66(epmc).pdf DeepDyve Pubget Overpricing