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10.4172/2167-1095.1000184 http://scihub22266oqcxt.onion/10.4172/2167-1095.1000184 C4501485!4501485 !26185735     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26185735 &cmd=llinks): Failed to open stream: HTTP request failed! 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The Role of Hypoxia-Inducible Factor/Prolyl Hydroxylation Pathway in Deoxycorticosterone Acetate/Salt Hypertension in the Rat |pdf=|usr=}}{{26185735 }} gab.com Text The Role of Hypoxia-Inducible Factor/Prolyl Hydroxylation Pathway in Deoxycorticosterone Acetate/Salt Hypertension in the Rat JO: J Hypertens (Los Angel) http://www.kidney.de/pget.php?&tw=1&pmid=26185735 #FOAvip KKidney disease could result from hypertension and ischemia/hypoxia. Key mediators of cellular adaptation to hypoxia are oxygen-sensitive hypoxia inducible factor (HIF)s which are regulated by prolyl-4-hydroxylase domain (PHD)-containing dioxygenases. However, HIF activation can be protective as in ischemic death or promote renal fibrosis in chronic conditions. This study tested the hypothesis that increased HIF-1? consequent to reduced PHD expression contributes to the attendant hypertension and target organ damage in deoxycorticosterone acetate (DOCA)/salt hypertension and that PHD inhibition ameliorates this effect. In rats made hypertensive by DOCA/salt treatment (DOCA 50 mg/kg s/c; 1% NaCl orally), PHD inhibition with dimethyl oxallyl glycine (DMOG) markedly attenuated hypertension (P<0.05), proteinuria (P<0.05) and attendant tubular interstitial changes and glomerular damage (P<0.05). Accompanying these changes, DMOG blunted the increased expression of kidney injury molecule (KIM)-1 (P<0.05), a marker of tubular injury and reversed the decreased expression of nephrin (P<0.05), a marker of glomerular injury. DMOG also decreased collagen I staining (P<0.05), increased serum nitrite (P<0.05) and decreased serum 8-isopostane (P<0.05). However, the increased HIF-1? expression (P<0.01) and decreased PHD2 expression (P<0.05) in DOCA/salt hypertensive rats was not affected by DMOG. These data suggest that reduced PHD2 expression with consequent increase in HIF-1? expression probably results from hypoxia induced by DOCA/salt treatment with the continued hypoxia and reduced PHD2 expression evoking hypertensive renal injury and collagen deposition at later stages. Moreover, a PHD inhibitor exerted a protective effect in DOCA/salt hypertension by mechanisms involving increased nitric oxide production and reduced production of reactive oxygen species. Twit Text FOAVip The Role of Hypoxia-Inducible Factor/Prolyl Hydroxylation Pathway in Deoxycorticosterone Acetate/Salt Hypertension in the Rat ????J Hypertens (Los Angel) http://www.kidney.de/pget.php?&tw=1&pmid=26185735 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26185735 #FOAvip English Wikipedia <ref>{{Cite pmid|26185735 }}</ref> The Role of Hypoxia-Inducible Factor/Prolyl Hydroxylation Pathway in Deoxycorticosterone Acetate/Salt Hypertension in the Rat #MMPMID26185735 Dallatu MK ; Nwokocha E ; Agu N ; Myung C ; Newaz MA ; Garcia G ; Truong LD ; Oyekan AO J Hypertens (Los Angel) 2014[Dec]; 3 (6 ): ä PMID26185735 show ga KKidney disease could result from hypertension and ischemia/hypoxia. Key mediators of cellular adaptation to hypoxia are oxygen-sensitive hypoxia inducible factor (HIF)s which are regulated by prolyl-4-hydroxylase domain (PHD)-containing dioxygenases. However, HIF activation can be protective as in ischemic death or promote renal fibrosis in chronic conditions. This study tested the hypothesis that increased HIF-1? consequent to reduced PHD expression contributes to the attendant hypertension and target organ damage in deoxycorticosterone acetate (DOCA)/salt hypertension and that PHD inhibition ameliorates this effect. In rats made hypertensive by DOCA/salt treatment (DOCA 50 mg/kg s/c; 1% NaCl orally), PHD inhibition with dimethyl oxallyl glycine (DMOG) markedly attenuated hypertension (P<0.05), proteinuria (P<0.05) and attendant tubular interstitial changes and glomerular damage (P<0.05). Accompanying these changes, DMOG blunted the increased expression of kidney injury molecule (KIM)-1 (P<0.05), a marker of tubular injury and reversed the decreased expression of nephrin (P<0.05), a marker of glomerular injury. DMOG also decreased collagen I staining (P<0.05), increased serum nitrite (P<0.05) and decreased serum 8-isopostane (P<0.05). However, the increased HIF-1? expression (P<0.01) and decreased PHD2 expression (P<0.05) in DOCA/salt hypertensive rats was not affected by DMOG. These data suggest that reduced PHD2 expression with consequent increase in HIF-1? expression probably results from hypoxia induced by DOCA/salt treatment with the continued hypoxia and reduced PHD2 expression evoking hypertensive renal injury and collagen deposition at later stages. Moreover, a PHD inhibitor exerted a protective effect in DOCA/salt hypertension by mechanisms involving increased nitric oxide production and reduced production of reactive oxygen species. äThe Role of Hypoxia-Inducible Factor/Prolyl Hydroxylation Pathway in (epmc).pdf DeepDyve Pubget Overpricing