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10.1161/HYPERTENSIONAHA.115.05314 http://scihub22266oqcxt.onion/10.1161/HYPERTENSIONAHA.115.05314 C4859813!4859813!25847948     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Hypertension 2015 ; 65 (6): 1307-15 Nephropedia Template TP {{tp|p=25847948|t=2015. Hypoxia-independent up-regulation of placental HIF-1? gene expression contributes to the pathogenesis of preeclampsia |pdf=|usr=}}{{25847948}} gab.com Text Hypoxia-independent up-regulation of placental HIF-1 gene expression contributes to the pathogenesis of preeclampsia JO: Hypertension http://www.kidney.de/pget.php?&tw=1&pmid=25847948 #FOAvip Accumulation of hypoxia inducible factor-1? (HIF-1?) is commonly an acute and beneficial response to hypoxia, while chronically elevated HIF-1? is associated with multiple disease conditions including preeclampsia (PE), a serious hypertensive disease of pregnancy. However, the molecular basis underlying the persistent elevation of placental HIF-1? in PE and its role in the pathogenesis of PE are poorly understood. Here we report that Hif-1? mRNA and HIF-1± protein were elevated in the placentas of pregnant mice infused with angiotensin II type I receptor agonistic autoantibody (AT1-AA), a pathogenic factor in PE. Knockdown of placental Hif-1? mRNA by specific siRNA significantly attenuated hallmark features of PE induced by AT1-AA in pregnant mice including hypertension, proteinuria, kidney damage, impaired placental vasculature, and elevated maternal circulating soluble fms-like tyrosine kinase-1 (sFlt-1) levels. Next, we discovered that Hif-1? mRNA levels and HIF-1± protein levels were induced in an independent PE model with infusion of the inflammatory cytokine LIGHT (tumor necrosis factor superfamily member 14). SiRNA knockdown experiments also demonstrated that elevated HIF-1? contributed to LIGHT-induced PE features. Translational studies with human placentas showed that AT1-AA or LIGHT is capable of inducing HIF-1? in a hypoxia-independent manner. Moreover, increased HIF-1? was found to be responsible for AT1-AA or LIGHT-induced elevation of Flt-1 gene expression and production of sFlt-1 in human villous explants. Overall, we demonstrated that hypoxia-independent stimulation of HIF-1? gene expression in the placenta is a common pathogenic mechanism promoting disease progression. Our findings reveal new insight to PE and highlight novel therapeutic possibilities for the disease. Twit Text FOAVip Hypoxia-independent up-regulation of placental HIF-1 gene expression contributes to the pathogenesis of preeclampsia ????Hypertension http://www.kidney.de/pget.php?&tw=1&pmid=25847948 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25847948 #FOAvip English Wikipedia <ref>{{Cite pmid|25847948}}</ref> Hypoxia-independent up-regulation of placental HIF-1? gene expression contributes to the pathogenesis of preeclampsia #MMPMID25847948 Iriyama T; Wang W; Parchim NF; Song A; Blackwell SC; Sibai BM; Kellems RE; Xia Y Hypertension 2015[Jun]; 65 (6): 1307-15 PMID25847948show ga Accumulation of hypoxia inducible factor-1? (HIF-1?) is commonly an acute and beneficial response to hypoxia, while chronically elevated HIF-1? is associated with multiple disease conditions including preeclampsia (PE), a serious hypertensive disease of pregnancy. However, the molecular basis underlying the persistent elevation of placental HIF-1? in PE and its role in the pathogenesis of PE are poorly understood. Here we report that Hif-1? mRNA and HIF-1± protein were elevated in the placentas of pregnant mice infused with angiotensin II type I receptor agonistic autoantibody (AT1-AA), a pathogenic factor in PE. Knockdown of placental Hif-1? mRNA by specific siRNA significantly attenuated hallmark features of PE induced by AT1-AA in pregnant mice including hypertension, proteinuria, kidney damage, impaired placental vasculature, and elevated maternal circulating soluble fms-like tyrosine kinase-1 (sFlt-1) levels. Next, we discovered that Hif-1? mRNA levels and HIF-1± protein levels were induced in an independent PE model with infusion of the inflammatory cytokine LIGHT (tumor necrosis factor superfamily member 14). SiRNA knockdown experiments also demonstrated that elevated HIF-1? contributed to LIGHT-induced PE features. Translational studies with human placentas showed that AT1-AA or LIGHT is capable of inducing HIF-1? in a hypoxia-independent manner. Moreover, increased HIF-1? was found to be responsible for AT1-AA or LIGHT-induced elevation of Flt-1 gene expression and production of sFlt-1 in human villous explants. Overall, we demonstrated that hypoxia-independent stimulation of HIF-1? gene expression in the placenta is a common pathogenic mechanism promoting disease progression. Our findings reveal new insight to PE and highlight novel therapeutic possibilities for the disease. äHypoxia-independent up-regulation of placental HIF-1? gene expression (epmc).pdf DeepDyve Pubget Overpricing