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10.1124/mol.114.092346 http://scihub22266oqcxt.onion/10.1124/mol.114.092346 C4164983!4164983 !25028481     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25028481 &cmd=llinks): Failed to open stream: HTTP request failed! 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G-protein ?? subunit dimers modulate kidney repair after ischemia-reperfusion injury in rats |pdf=|usr=}}{{25028481 }} gab.com Text G-protein subunit dimers modulate kidney repair after ischemia-reperfusion injury in rats JO: Mol Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=25028481 #FOAvip Heterotrimeric G-proteins play a crucial role in the control of renal epithelial cell function during homeostasis and in response to injury. In this report, G-protein ?? subunit (G??) dimer activity was evaluated during the process of tubular repair after renal ischemia-reperfusion injury (IRI) in male Sprague Dawley rats. Rats were treated with a small molecule inhibitor of G?? activity, gallein (30 or 100 mg/kg), 1 hour after reperfusion and every 24 hours for 3 additional days. After IRI, renal dysfunction was prolonged after the high-dose gallein treatment in comparison with vehicle treatment during the 7-day recovery period. Renal tubular repair in the outer medulla 7 days after IRI was significantly (P < 0.001) attenuated after treatment with high-dose gallein (100 mg/kg) in comparison with low-dose gallein (30 mg/kg), or the vehicle and fluorescein control groups. Gallein treatment significantly reduced (P < 0.05) the number of proliferating cell nuclear antigen-positive tubular epithelial cells at 24 hours after the ischemia-reperfusion phase in vivo. In vitro application of gallein on normal rat kidney (NRK-52E) proximal tubule cells significantly reduced (P < 0.05) S-phase cell cycle entry compared with vehicle-treated cells as determined by 5'-bromo-2'-deoxyuridine incorporation. Taken together, these data suggest that G?? signaling contributes to the maintenance and repair of renal tubular epithelium and may be a novel therapeutic target for the development of drugs to treat acute kidney injury. Twit Text FOAVip G-protein subunit dimers modulate kidney repair after ischemia-reperfusion injury in rats ????Mol Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=25028481 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25028481 #FOAvip English Wikipedia <ref>{{Cite pmid|25028481 }}</ref> G-protein ?? subunit dimers modulate kidney repair after ischemia-reperfusion injury in rats #MMPMID25028481 White SM ; North LM ; Haines E ; Goldberg M ; Sullivan LM ; Pressly JD ; Weber DS ; Park F ; Regner KR Mol Pharmacol 2014[Oct]; 86 (4 ): 369-77 PMID25028481 show ga Heterotrimeric G-proteins play a crucial role in the control of renal epithelial cell function during homeostasis and in response to injury. In this report, G-protein ?? subunit (G??) dimer activity was evaluated during the process of tubular repair after renal ischemia-reperfusion injury (IRI) in male Sprague Dawley rats. Rats were treated with a small molecule inhibitor of G?? activity, gallein (30 or 100 mg/kg), 1 hour after reperfusion and every 24 hours for 3 additional days. After IRI, renal dysfunction was prolonged after the high-dose gallein treatment in comparison with vehicle treatment during the 7-day recovery period. Renal tubular repair in the outer medulla 7 days after IRI was significantly (P < 0.001) attenuated after treatment with high-dose gallein (100 mg/kg) in comparison with low-dose gallein (30 mg/kg), or the vehicle and fluorescein control groups. Gallein treatment significantly reduced (P < 0.05) the number of proliferating cell nuclear antigen-positive tubular epithelial cells at 24 hours after the ischemia-reperfusion phase in vivo. In vitro application of gallein on normal rat kidney (NRK-52E) proximal tubule cells significantly reduced (P < 0.05) S-phase cell cycle entry compared with vehicle-treated cells as determined by 5'-bromo-2'-deoxyuridine incorporation. Taken together, these data suggest that G?? signaling contributes to the maintenance and repair of renal tubular epithelium and may be a novel therapeutic target for the development of drugs to treat acute kidney injury. |Animals [MESH] |Cardio-Renal Syndrome/*drug therapy/metabolism [MESH] |Cell Line [MESH] |Cell Movement [MESH] |Cell Proliferation [MESH] |Epithelial Cells/drug effects/metabolism/physiology [MESH] |GTP-Binding Protein beta Subunits/antagonists & inhibitors/*metabolism [MESH] |GTP-Binding Protein gamma Subunits/antagonists & inhibitors/*metabolism [MESH] |Kidney/*drug effects/metabolism/pathology [MESH] |Male [MESH] |Protein Multimerization [MESH] |Rats [MESH] |Rats, Sprague-Dawley [MESH] |Reperfusion Injury/drug therapy/*metabolism [MESH]G-protein ?? subunit dimers modulate kidney repair after ischemia-repe(epmc).pdf DeepDyve Pubget Overpricing