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10.1152/ajpregu.00370.2017 http://scihub22266oqcxt.onion/10.1152/ajpregu.00370.2017 29212810!5899255!29212810     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Am+J+Physiol+Regul+Integr+Comp+Physiol 2018 ; 314 (3): R427-R432 Nephropedia Template TP {{tp|p=29212810|t=2018. Heme oxygenase-1 is a potent inhibitor of placental ischemia-mediated endothelin-1 production in cultured human glomerular endothelial cells |pdf=|usr=}}{{29212810}} gab.com Text Heme oxygenase-1 is a potent inhibitor of placental ischemia-mediated endothelin-1 production in cultured human glomerular endothelial cells JO: Am J Physiol Regul Integr Comp Physiol http://www.kidney.de/pget.php?&tw=1&pmid=29212810 #FOAvip Preeclampsia is a pregnancy-specific disorder of maternal hypertension and reduced renal hemodynamics linked to reduced endothelial function. Placental ischemia is thought to be the culprit of this disease, as it causes the release of factors like tumor necrosis factor (TNF)-alpha that induce vascular endothelin-1 (ET-1) production. Interestingly, placental ischemia-induced hypertension in rats [reduced uterine perfusion pressure (RUPP) model] is abolished by ET(A) receptor blockade, suggesting a critical role for ET-1. Although it has been found that systemic induction of heme oxygenase (HO)-1 is associated with reduced ET-1 production and attenuated hypertension, it is unclear whether HO-1 directly modulates the increased ET-1 response to placental factors. We tested the hypothesis that HO-1 or its metabolites inhibit ET-1 production in human glomerular endothelial cells induced by serum of RUPP rats or TNF-alpha. Serum (5%) from RUPP hypertensive (mean arterial blood pressure 119 +/- 9 mmHg) vs. normotensive pregnant (NP, 101 +/- 6 mmHg, P < 0.001) rats increased ET-1 production (RUPP 168.8 +/- 18.1 pg/ml, NP 80.3 +/- 22.7 pg/ml, P < 0.001, n = 12/group). HO-1 induction [25 microM cobalt photoporphyrin (CoPP)] abolished RUPP serum-induced ET-1 production (1.6 +/- 0.8 pg/ml, P < 0.001), whereas bilirubin (10 microM) significantly attenuated ET-1 release (125.3 +/- 5.2 pg/ml, P = 0.005). Furthermore, TNF-alpha-induced ET-1 production (TNF-alpha 31.0 +/- 8.4 vs. untreated 7.5 +/- 0.4 pg/ml, P < 0.001) was reduced by CoPP (1.5 +/- 0.8 pg/ml, P < 0.001) and bilirubin (10.5 +/- 4.3 pg/ml, P < 0.001). These results suggest that circulating factors released during placental ischemia target the maternal glomerular endothelium to increase ET-1, and that pharmacological induction of HO-1 or bilirubin could be a treatment strategy to block this prohypertensive pathway in preeclampsia. Twit Text FOAVip Heme oxygenase-1 is a potent inhibitor of placental ischemia-mediated endothelin-1 production in cultured human glomerular endothelial cells ????Am J Physiol Regul Integr Comp Physiol http://www.kidney.de/pget.php?&tw=1&pmid=29212810 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29212810 #FOAvip English Wikipedia <ref>{{Cite pmid|29212810}}</ref> Heme oxygenase-1 is a potent inhibitor of placental ischemia-mediated endothelin-1 production in cultured human glomerular endothelial cells #MMPMID29212810 Bakrania BA; Spradley FT; Satchell SC; Stec DE; Rimoldi JM; Gadepalli RSV; Granger JP Am J Physiol Regul Integr Comp Physiol 2018[Mar]; 314 (3): R427-R432 PMID29212810show ga Preeclampsia is a pregnancy-specific disorder of maternal hypertension and reduced renal hemodynamics linked to reduced endothelial function. Placental ischemia is thought to be the culprit of this disease, as it causes the release of factors like tumor necrosis factor (TNF)-alpha that induce vascular endothelin-1 (ET-1) production. Interestingly, placental ischemia-induced hypertension in rats [reduced uterine perfusion pressure (RUPP) model] is abolished by ET(A) receptor blockade, suggesting a critical role for ET-1. Although it has been found that systemic induction of heme oxygenase (HO)-1 is associated with reduced ET-1 production and attenuated hypertension, it is unclear whether HO-1 directly modulates the increased ET-1 response to placental factors. We tested the hypothesis that HO-1 or its metabolites inhibit ET-1 production in human glomerular endothelial cells induced by serum of RUPP rats or TNF-alpha. Serum (5%) from RUPP hypertensive (mean arterial blood pressure 119 +/- 9 mmHg) vs. normotensive pregnant (NP, 101 +/- 6 mmHg, P < 0.001) rats increased ET-1 production (RUPP 168.8 +/- 18.1 pg/ml, NP 80.3 +/- 22.7 pg/ml, P < 0.001, n = 12/group). HO-1 induction [25 microM cobalt photoporphyrin (CoPP)] abolished RUPP serum-induced ET-1 production (1.6 +/- 0.8 pg/ml, P < 0.001), whereas bilirubin (10 microM) significantly attenuated ET-1 release (125.3 +/- 5.2 pg/ml, P = 0.005). Furthermore, TNF-alpha-induced ET-1 production (TNF-alpha 31.0 +/- 8.4 vs. untreated 7.5 +/- 0.4 pg/ml, P < 0.001) was reduced by CoPP (1.5 +/- 0.8 pg/ml, P < 0.001) and bilirubin (10.5 +/- 4.3 pg/ml, P < 0.001). These results suggest that circulating factors released during placental ischemia target the maternal glomerular endothelium to increase ET-1, and that pharmacological induction of HO-1 or bilirubin could be a treatment strategy to block this prohypertensive pathway in preeclampsia. |*Placental Circulation[MESH] |Animals[MESH] |Arterial Pressure[MESH] |Bilirubin/pharmacology[MESH] |Biliverdine/pharmacology[MESH] |Boranes/pharmacology[MESH] |Carbonates/pharmacology[MESH] |Cells, Cultured[MESH] |Disease Models, Animal[MESH] |Endothelial Cells/drug effects/*enzymology[MESH] |Endothelin-1/*metabolism[MESH] |Enzyme Induction[MESH] |Female[MESH] |Heme Oxygenase-1/*metabolism[MESH] |Ischemia/blood/*enzymology/physiopathology[MESH] |Kidney Glomerulus/drug effects/*enzymology[MESH] |Placenta/*blood supply[MESH] |Pre-Eclampsia/blood/*enzymology/physiopathology[MESH] |Pregnancy[MESH] |Protoporphyrins/pharmacology[MESH] |Rats, Sprague-Dawley[MESH]Heme oxygenase-1 is a potent inhibitor of placental ischemia-mediated (epmc).pdf DeepDyve Pubget Overpricing