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10.1152/ajpregu.00566.2013 http://scihub22266oqcxt.onion/10.1152/ajpregu.00566.2013 24553299!4010664!24553299     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24553299&cmd=llinks): Failed to open stream: HTTP request failed! 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Heme oxygenase-1 promotes migration and beta-epithelial Na+ channel expression in cytotrophoblasts and ischemic placentas |pdf=|usr=}}{{24553299}} gab.com Text Heme oxygenase-1 promotes migration and beta-epithelial Na+ channel expression in cytotrophoblasts and ischemic placentas JO: Am J Physiol Regul Integr Comp Physiol http://www.kidney.de/pget.php?&tw=1&pmid=24553299 #FOAvip Preeclampsia is thought to arise from inadequate cytotrophoblast migration and invasion of the maternal spiral arteries, resulting in placental ischemia and hypertension. Evidence suggests that altered expression of epithelial Na(+) channel (ENaC) proteins may be a contributing mechanism for impaired cytotrophoblast migration. ENaC activity is required for normal cytotrophoblast migration. Moreover, beta-ENaC, the most robustly expressed placental ENaC message, is reduced in placentas from preeclamptic women. We recently demonstrated that heme oxygenase-1 (HO-1) protects against hypertension in a rat model of placental ischemia; however, whether HO-1 regulation of beta-ENaC contributes to the beneficial effects of HO-1 is unknown. The purpose of this study was to determine whether beta-ENaC mediates cytotrophoblast migration and whether HO-1 enhances ENaC-mediated migration. We showed that placental ischemia, induced by reducing uterine perfusion suppressed, and HO-1 induction restored, beta-ENaC expression in ischemic placentas. Using an in vitro model, we found that HO-1 induction, using cobalt protoporphyrin, stimulates cytotrophoblast beta-ENaC expression by 1.5- and 1.8-fold (10 and 50 muM). We then showed that silencing of beta-ENaC in cultured cytotrophoblasts (BeWo cells), by expression of dominant-negative constructs, reduced migration to 56 +/- 13% (P < 0.05) of control. Importantly, HO-1 induction enhanced migration (43 +/- 5% of control, P < 0.05), but the enhanced migratory response was entirely blocked by ENaC inhibition with amiloride (10 muM). Taken together, our results suggest that beta-ENaC mediates cytotrophoblast migration and increasing beta-ENaC expression by HO-1 induction enhances migration. HO-1 regulation of cytotrophoblast beta-ENaC expression and migration may be a potential therapeutic target in preeclamptic patients. Twit Text FOAVip Heme oxygenase-1 promotes migration and beta-epithelial Na+ channel expression in cytotrophoblasts and ischemic placentas ????Am J Physiol Regul Integr Comp Physiol http://www.kidney.de/pget.php?&tw=1&pmid=24553299 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24553299 #FOAvip English Wikipedia <ref>{{Cite pmid|24553299}}</ref> Heme oxygenase-1 promotes migration and beta-epithelial Na+ channel expression in cytotrophoblasts and ischemic placentas #MMPMID24553299 Warrington JP; Coleman K; Skaggs C; Hosick PA; George EM; Stec DE; Ryan MJ; Granger JP; Drummond HA Am J Physiol Regul Integr Comp Physiol 2014[May]; 306 (9): R641-6 PMID24553299show ga Preeclampsia is thought to arise from inadequate cytotrophoblast migration and invasion of the maternal spiral arteries, resulting in placental ischemia and hypertension. Evidence suggests that altered expression of epithelial Na(+) channel (ENaC) proteins may be a contributing mechanism for impaired cytotrophoblast migration. ENaC activity is required for normal cytotrophoblast migration. Moreover, beta-ENaC, the most robustly expressed placental ENaC message, is reduced in placentas from preeclamptic women. We recently demonstrated that heme oxygenase-1 (HO-1) protects against hypertension in a rat model of placental ischemia; however, whether HO-1 regulation of beta-ENaC contributes to the beneficial effects of HO-1 is unknown. The purpose of this study was to determine whether beta-ENaC mediates cytotrophoblast migration and whether HO-1 enhances ENaC-mediated migration. We showed that placental ischemia, induced by reducing uterine perfusion suppressed, and HO-1 induction restored, beta-ENaC expression in ischemic placentas. Using an in vitro model, we found that HO-1 induction, using cobalt protoporphyrin, stimulates cytotrophoblast beta-ENaC expression by 1.5- and 1.8-fold (10 and 50 muM). We then showed that silencing of beta-ENaC in cultured cytotrophoblasts (BeWo cells), by expression of dominant-negative constructs, reduced migration to 56 +/- 13% (P < 0.05) of control. Importantly, HO-1 induction enhanced migration (43 +/- 5% of control, P < 0.05), but the enhanced migratory response was entirely blocked by ENaC inhibition with amiloride (10 muM). Taken together, our results suggest that beta-ENaC mediates cytotrophoblast migration and increasing beta-ENaC expression by HO-1 induction enhances migration. HO-1 regulation of cytotrophoblast beta-ENaC expression and migration may be a potential therapeutic target in preeclamptic patients. |*Cell Movement[MESH] |Animals[MESH] |Cell Line, Tumor[MESH] |Disease Models, Animal[MESH] |Enzyme Induction[MESH] |Epithelial Sodium Channels/genetics/*metabolism[MESH] |Female[MESH] |Heme Oxygenase (Decyclizing)/biosynthesis/*metabolism[MESH] |Heme Oxygenase-1/biosynthesis/*metabolism[MESH] |Humans[MESH] |Ischemia/*enzymology/physiopathology[MESH] |Placenta/*blood supply/*enzymology[MESH] |Placental Circulation[MESH] |Pre-Eclampsia/metabolism/physiopathology[MESH] |Pregnancy[MESH] |RNA Interference[MESH] |Rats[MESH] |Rats, Sprague-Dawley[MESH] |Signal Transduction[MESH] |Transfection[MESH]Heme oxygenase-1 promotes migration and beta-epithelial Na+ channel ex(epmc).pdf DeepDyve Pubget Overpricing