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10.1152/ajprenal.00066.2015 http://scihub22266oqcxt.onion/10.1152/ajprenal.00066.2015 C4469889!4469889!25925251     free     free     free Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Am+J+Physiol+Renal+Physiol 2015 ; 308 (12): F1452-62 Nephropedia Template TP {{tp|p=25925251|t=2015. Muc1 is protective during kidney ischemia-reperfusion injury |pdf=|usr=}}{{25925251}} gab.com Text Muc1 is protective during kidney ischemia-reperfusion injury JO: Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=25925251 #FOAvip Ischemia-reperfusion injury (IRI) due to hypotension is a common cause of human acute kidney injury (AKI). Hypoxia-inducible transcription factors (HIFs) orchestrate a protective response in renal endothelial and epithelial cells in AKI models. As human mucin 1 (MUC1) is induced by hypoxia and enhances HIF-1 activity in cultured epithelial cells, we asked whether mouse mucin 1 (Muc1) regulates HIF-1 activity in kidney tissue during IRI. Whereas Muc1 was localized on the apical surface of the thick ascending limb, distal convoluted tubule, and collecting duct in the kidneys of sham-treated mice, Muc1 appeared in the cytoplasm and nucleus of all tubular epithelia during IRI. Muc1 was induced during IRI, and Muc1 transcripts and protein were also present in recovering proximal tubule cells. Kidney damage was worse and recovery was blocked during IRI in Muc1 knockout mice compared with congenic control mice. Muc1 knockout mice had reduced levels of HIF-1?, reduced or aberrant induction of HIF-1 target genes involved in the shift of glucose metabolism to glycolysis, and prolonged activation of AMP-activated protein kinase, indicating metabolic stress. Muc1 clearly plays a significant role in enhancing the HIF protective pathway during ischemic insult and recovery in kidney epithelia, providing a new target for developing therapies to treat AKI. Moreover, our data support a role specifically for HIF-1 in epithelial protection of the kidney during IRI as Muc1 is present only in tubule epithelial cells. Twit Text FOAVip Muc1 is protective during kidney ischemia-reperfusion injury ????Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=25925251 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25925251 #FOAvip English Wikipedia <ref>{{Cite pmid|25925251}}</ref> Muc1 is protective during kidney ischemia-reperfusion injury #MMPMID25925251 Pastor-Soler NM; Sutton TA; Mang HE; Kinlough CL; Gendler SJ; Madsen CS; Bastacky SI; Ho J; Al-bataineh MM; Hallows KR; Singh S; Monga SP; Kobayashi H; Haase VH; Hughey RP Am J Physiol Renal Physiol 2015[Jun]; 308 (12): F1452-62 PMID25925251show ga Ischemia-reperfusion injury (IRI) due to hypotension is a common cause of human acute kidney injury (AKI). Hypoxia-inducible transcription factors (HIFs) orchestrate a protective response in renal endothelial and epithelial cells in AKI models. As human mucin 1 (MUC1) is induced by hypoxia and enhances HIF-1 activity in cultured epithelial cells, we asked whether mouse mucin 1 (Muc1) regulates HIF-1 activity in kidney tissue during IRI. Whereas Muc1 was localized on the apical surface of the thick ascending limb, distal convoluted tubule, and collecting duct in the kidneys of sham-treated mice, Muc1 appeared in the cytoplasm and nucleus of all tubular epithelia during IRI. Muc1 was induced during IRI, and Muc1 transcripts and protein were also present in recovering proximal tubule cells. Kidney damage was worse and recovery was blocked during IRI in Muc1 knockout mice compared with congenic control mice. Muc1 knockout mice had reduced levels of HIF-1?, reduced or aberrant induction of HIF-1 target genes involved in the shift of glucose metabolism to glycolysis, and prolonged activation of AMP-activated protein kinase, indicating metabolic stress. Muc1 clearly plays a significant role in enhancing the HIF protective pathway during ischemic insult and recovery in kidney epithelia, providing a new target for developing therapies to treat AKI. Moreover, our data support a role specifically for HIF-1 in epithelial protection of the kidney during IRI as Muc1 is present only in tubule epithelial cells. äMuc1 is protective during kidney ischemia-reperfusion injury (epmc).pdf DeepDyve Pubget Overpricing