Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.3892/ijmm.2017.2957 http://scihub22266oqcxt.onion/10.3892/ijmm.2017.2957 C5428938!5428938 !28440394     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\28440394 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Int+J+Mol+Med 2017 ; 39 (6 ): 1461-1467 Nephropedia Template TP {{tp|p=28440394 |t=2017. G-protein-coupled receptor 30 mediates the effects of estrogen on endothelial cell tube formation in vitro |pdf=|usr=}}{{28440394 }} gab.com Text G-protein-coupled receptor 30 mediates the effects of estrogen on endothelial cell tube formation in vitro JO: Int J Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=28440394 #FOAvip The placenta is the exchange organ between the mother and the fetus. The inadequate function of this organ is associated with a number of pregnancy disorders. Hypoxia and oxidative stress during placental development may induce endothelial dysfunction, resulting in the reduction in the perfusion of the placenta. During pregnancy, the levels of estrogen are increased. Decreased estrogen levels have been reported in women with preeclampsia. However, whether estrogen is involved in placental angiogenesis remains unclear. In this study, we aimed to investigate the effects of estrogen on endothelial cell tube formation and to elucidate the underlying mechanisms. For this purpose, human umbilical vein endothelial cells (HUVECs) were cultured with 17???estradiol under conditions of hypoxia/reoxygenation (H/R). The total pipe length of the tube?like structure on endothelial cells was measured. The expression levels of G?protein?coupled receptor 30 (GPR30) and endothelial nitric oxide synthase (eNOS) and Akt were also measured in the endothelial cells following treatment with 17???estradiol under H/R conditions by western blot analysis and immunostaining. We found that the total pipe length of the tube?like structure on endothelial cells was significantly reduced. This reduction was reversed by treatment with 17???estradiol. The expression of GPR30 in endothelial cells was significantly increased following treatment with 17???estradiol under H/R conditions. Furthermore, the levels of eNOS and Akt in endothelial cells were also significantly increased following treatment with 17-?-estradiol under H/R conditions. The activation of eNOS was inhibited by wortmannin, an inhibitor of PI3K/Akt. Our data thus demonstrate that estrogen prevents the failure of endothelial cell tube formation induced by H/R. GPR30 plays an important role in these protective effects through the activation of eNOS and Akt in endothelial cells. Our data suggest that increased levels of estrogen are important for placental angiogenesis. Twit Text FOAVip G-protein-coupled receptor 30 mediates the effects of estrogen on endothelial cell tube formation in vitro ????Int J Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=28440394 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28440394 #FOAvip English Wikipedia <ref>{{Cite pmid|28440394 }}</ref> G-protein-coupled receptor 30 mediates the effects of estrogen on endothelial cell tube formation in vitro #MMPMID28440394 Zhou L ; Chen H ; Mao X ; Qi H ; Baker PN ; Zhang H Int J Mol Med 2017[Jun]; 39 (6 ): 1461-1467 PMID28440394 show ga The placenta is the exchange organ between the mother and the fetus. The inadequate function of this organ is associated with a number of pregnancy disorders. Hypoxia and oxidative stress during placental development may induce endothelial dysfunction, resulting in the reduction in the perfusion of the placenta. During pregnancy, the levels of estrogen are increased. Decreased estrogen levels have been reported in women with preeclampsia. However, whether estrogen is involved in placental angiogenesis remains unclear. In this study, we aimed to investigate the effects of estrogen on endothelial cell tube formation and to elucidate the underlying mechanisms. For this purpose, human umbilical vein endothelial cells (HUVECs) were cultured with 17???estradiol under conditions of hypoxia/reoxygenation (H/R). The total pipe length of the tube?like structure on endothelial cells was measured. The expression levels of G?protein?coupled receptor 30 (GPR30) and endothelial nitric oxide synthase (eNOS) and Akt were also measured in the endothelial cells following treatment with 17???estradiol under H/R conditions by western blot analysis and immunostaining. We found that the total pipe length of the tube?like structure on endothelial cells was significantly reduced. This reduction was reversed by treatment with 17???estradiol. The expression of GPR30 in endothelial cells was significantly increased following treatment with 17???estradiol under H/R conditions. Furthermore, the levels of eNOS and Akt in endothelial cells were also significantly increased following treatment with 17-?-estradiol under H/R conditions. The activation of eNOS was inhibited by wortmannin, an inhibitor of PI3K/Akt. Our data thus demonstrate that estrogen prevents the failure of endothelial cell tube formation induced by H/R. GPR30 plays an important role in these protective effects through the activation of eNOS and Akt in endothelial cells. Our data suggest that increased levels of estrogen are important for placental angiogenesis. |*Neovascularization, Physiologic [MESH] |Cell Hypoxia [MESH] |Endothelial Cells/cytology/*metabolism [MESH] |Estradiol/*metabolism [MESH] |Human Umbilical Vein Endothelial Cells [MESH] |Humans [MESH] |Hypoxia/metabolism [MESH] |Nitric Oxide Synthase Type III/metabolism [MESH] |Oxidative Stress [MESH] |Proto-Oncogene Proteins c-akt/metabolism [MESH] |Receptors, Estrogen/*metabolism [MESH]G-protein-coupled receptor 30 mediates the effects of estrogen on endo(epmc).pdf DeepDyve Pubget Overpricing