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10.4103/0366-6999.204112 http://scihub22266oqcxt.onion/10.4103/0366-6999.204112 C5407042!5407042!28397725     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 278.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 278.79999999999995 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\28397725.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Chin+Med+J+(Engl) 2017 ; 130 (8): 950-6 Nephropedia Template TP {{tp|p=28397725|t=2017. Transforming Growth Factor-beta 1 Involved in the Pathogenesis of Endometriosis through Regulating Expression of Vascular Endothelial Growth Factor under Hypoxia |pdf=|usr=}}{{28397725}} gab.com Text Transforming Growth Factor-beta 1 Involved in the Pathogenesis of Endometriosis through Regulating Expression of Vascular Endothelial Growth Factor under Hypoxia JO: Chin Med J (Engl) http://www.kidney.de/pget.php?&tw=1&pmid=28397725 #FOAvip Background:: Endometriosis (EMs) is a common gynecological disorder characterized by endometrial-like tissue outside the uterus. Hypoxia induces the expression of many important downstream genes to regulate the implantation, survival, and maintenance of ectopic endometriotic lesions. Transforming growth factor-beta 1 (TGF-?1) plays a major role in the etiology of EMs. We aimed to determine whether TGF-?1 affects EMs development and progression and its related mechanisms in hypoxic conditions. Methods:: Endometrial tissue was obtained from women with or without EMs undergoing surgery from October, 2015 to October, 2016. Endometrial cells were cultured and then exposed to hypoxia and TGF-?1 or TGF-?1 inhibitors. The messenger RNA (mRNA) and protein expression levels of TGF-?1, vascular endothelial growth factor (VEGF), and hypoxia-inducible factor-1? (HIF-1?) were measured. A Dual-Luciferase Reporter Assay was used to examine the effect of TGF-?1 and hypoxia on a VEGF promoter construct. Student's t-test was performed for comparison among groups (one-sided or two-sided) and a value of P < 0.05 was considered statistically significant. Results:: TGF-?1, VEGF, HIF-1? mRNA, and protein expression were significantly higher in EMs tissue than that in normal endometrial tissue (t = 2.16, P = 0.042). EMs primary cultured cells exposed to hypoxia expressed 43.8% higher VEGF mRNA and protein (t = 6.84, P = 0.023). VEGF mRNA levels increased 12.5% in response to TGF-?, whereas the combined treatment of hypoxia/TGF-?1 resulted in a much higher production (87.5% increases) of VEGF. The luciferase activity of the VEGF promoter construct was increased in the presence of either TGF-?1 (2.6-fold, t = 6.08, P = 0.032) or hypoxia (11.2-fold, t = 32.70, P < 0.001), whereas the simultaneous presence of both stimuli resulted in a significant cooperative effect (18.5-fold, t = 33.50, P < 0.001). Conclusions:: The data support the hypothesis that TGF-?1 is involved in the pathogenesis of EMs through regulating VEGF expression. An additive effect of TGF-?1 and hypoxia is taking place at the transcriptional level. Twit Text FOAVip Transforming Growth Factor-beta 1 Involved in the Pathogenesis of Endometriosis through Regulating Expression of Vascular Endothelial Growth Factor under Hypoxia ????Chin Med J (Engl) http://www.kidney.de/pget.php?&tw=1&pmid=28397725 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28397725 #FOAvip English Wikipedia <ref>{{Cite pmid|28397725}}</ref> Transforming Growth Factor-beta 1 Involved in the Pathogenesis of Endometriosis through Regulating Expression of Vascular Endothelial Growth Factor under Hypoxia #MMPMID28397725 Yu YX; Xiu YL; Chen X; Li YL Chin Med J (Engl) 2017[Apr]; 130 (8): 950-6 PMID28397725show ga Background:: Endometriosis (EMs) is a common gynecological disorder characterized by endometrial-like tissue outside the uterus. Hypoxia induces the expression of many important downstream genes to regulate the implantation, survival, and maintenance of ectopic endometriotic lesions. Transforming growth factor-beta 1 (TGF-?1) plays a major role in the etiology of EMs. We aimed to determine whether TGF-?1 affects EMs development and progression and its related mechanisms in hypoxic conditions. Methods:: Endometrial tissue was obtained from women with or without EMs undergoing surgery from October, 2015 to October, 2016. Endometrial cells were cultured and then exposed to hypoxia and TGF-?1 or TGF-?1 inhibitors. The messenger RNA (mRNA) and protein expression levels of TGF-?1, vascular endothelial growth factor (VEGF), and hypoxia-inducible factor-1? (HIF-1?) were measured. A Dual-Luciferase Reporter Assay was used to examine the effect of TGF-?1 and hypoxia on a VEGF promoter construct. Student's t-test was performed for comparison among groups (one-sided or two-sided) and a value of P < 0.05 was considered statistically significant. Results:: TGF-?1, VEGF, HIF-1? mRNA, and protein expression were significantly higher in EMs tissue than that in normal endometrial tissue (t = 2.16, P = 0.042). EMs primary cultured cells exposed to hypoxia expressed 43.8% higher VEGF mRNA and protein (t = 6.84, P = 0.023). VEGF mRNA levels increased 12.5% in response to TGF-?, whereas the combined treatment of hypoxia/TGF-?1 resulted in a much higher production (87.5% increases) of VEGF. The luciferase activity of the VEGF promoter construct was increased in the presence of either TGF-?1 (2.6-fold, t = 6.08, P = 0.032) or hypoxia (11.2-fold, t = 32.70, P < 0.001), whereas the simultaneous presence of both stimuli resulted in a significant cooperative effect (18.5-fold, t = 33.50, P < 0.001). Conclusions:: The data support the hypothesis that TGF-?1 is involved in the pathogenesis of EMs through regulating VEGF expression. An additive effect of TGF-?1 and hypoxia is taking place at the transcriptional level. äTransforming Growth Factor-beta 1 Involved in the Pathogenesis of Endo(epmc).pdf DeepDyve Pubget Overpricing