OBJECTIVE: To determine whether 17beta-estradiol (E(2)) and selective estrogen receptor modulators can regulate vascular endothelial growth factor (VEGF) and soluble VEGF receptor 1 (sVEGFR-1) as a VEGF antagonist in human endometrial stromal cells (ESCs). DESIGN: In vitro experiment. SETTING: Research laboratory at Kansai Medical University. PATIENT(S): Sixteen patients undergoing hysterectomy for benign reasons. INTERVENTION(S): The ESCs were cultured with E(2), 4-hydroxytamoxifen (OHT), and raloxifene. MAIN OUTCOME MEASURE(S): The VEGF and sVEGFR-1 messenger RNA (mRNA) levels in ESCs were determined using quantitative real-time reverse transcriptase-polymerase chain reaction (RT-PCR). Free (unbound) VEGF and sVEGFR-1 protein levels from ESCs were measured using ELISA kits. RESULT(S): The E(2) significantly induced VEGF mRNA levels, whereas E2 caused a significant decrease in sVEGFR-1 messenger RNA (mRNA) levels. The E(2) or OHT significantly increased the VEGF production levels and attenuated the sVEGFR-1 production compared with control, but raloxifene had no significant effect. The decrease in levels of free VEGF was proportional to the increase in sVEGFR-1 levels in the culture media of ESCs. CONCLUSION(S): The E(2) or OHT stimulates VEGF production and concurrently attenuates sVEGFR-1 production in ESCs. This consequential increase in VEGF:sVEGFR-1 ratio might enhance the biological effects of VEGF on the angiogenic environment in human endometrium. Copyright 2010 American Society for Reproductive Medicine. Published by Elsevier Inc. All rights reserved.
OBJECTIVE: To determine whether 17beta-estradiol (E(2)) and selective estrogen receptor modulators can regulate vascular endothelial growth factor (VEGF) and soluble VEGF receptor 1 (sVEGFR-1) as a VEGF antagonist in human endometrial stromal cells (ESCs). DESIGN: In vitro experiment. SETTING: Research laboratory at Kansai Medical University. PATIENT(S): Sixteen patients undergoing hysterectomy for benign reasons. INTERVENTION(S): The ESCs were cultured with E(2), 4-hydroxytamoxifen (OHT), and raloxifene. MAIN OUTCOME MEASURE(S): The VEGF and sVEGFR-1 messenger RNA (mRNA) levels in ESCs were determined using quantitative real-time reverse transcriptase-polymerase chain reaction (RT-PCR). Free (unbound) VEGF and sVEGFR-1 protein levels from ESCs were measured using ELISA kits. RESULT(S): The E(2) significantly induced VEGF mRNA levels, whereas E2 caused a significant decrease in sVEGFR-1 messenger RNA (mRNA) levels. The E(2) or OHT significantly increased the VEGF production levels and attenuated the sVEGFR-1 production compared with control, but raloxifene had no significant effect. The decrease in levels of free VEGF was proportional to the increase in sVEGFR-1 levels in the culture media of ESCs. CONCLUSION(S): The E(2) or OHT stimulates VEGF production and concurrently attenuates sVEGFR-1 production in ESCs. This consequential increase in VEGF:sVEGFR-1 ratio might enhance the biological effects of VEGF on the angiogenic environment in human endometrium. Copyright 2010 American Society for Reproductive Medicine. Published by Elsevier Inc. All rights reserved.
Authors: Alison B Edelman; Bliss Kaneshiro; Katharine B Simmons; Jennifer L Hauschildt; Kise Bond; Emily R Boniface; Jeffrey T Jensen Journal: Obstet Gynecol Date: 2020-08 Impact factor: 7.623
Authors: Chun-E Ren; Xueqiong Zhu; Jinping Li; Christian Lyle; Sean Dowdy; Karl C Podratz; David Byck; Hai-Bin Chen; Shi-Wen Jiang Journal: Int J Mol Sci Date: 2015-03-13 Impact factor: 5.923