Tan Z, Yang D, Lu W
Department of Physiology, Sun Yat-sen University of Medical Sciences, Guangzhou 510089, China.
Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2001 Aug;17(3):251-4.
To determine the effect of 17 beta-estradiol on proliferation of cultured vascular smooth muscle cells (VSMC) and expression of ET(A) receptor mRNA stimulated by endothelin-1 (ET-1). The experimental models of proliferation in cultured rat aortic smooth muscle cells induced by ET-1 was established. The 3H-thymidine ([3H]-TdR) incorporation, cell counts and reverse transcription-polymerase chain reaction (RT-PCR) were used in this study.
BQ123, the selective ET(A) receptor antagonist, inhibited the increase of [3H]-TdR incorporation and cell number in response to ET-1 of VSMC.17 beta-estradiol may reverse the increase of [3H] TdR incorporation and cell number stimulated by ET-1. 17 beta-estradiol downregulated of ET(A) receptor mRNA expression, with the maximum at 12 hours, which was partially prevented by tamoxifen, an estrogen receptor antagonist.
The proliferation of VSMC stimulated by ET-1 was mainly through ET(A) receptor. 17 beta-estradiol inhibited the proliferation of VSMC stimulated by ET-1, which might be through downregulation of ET(A) receptor.
确定17β-雌二醇对培养的血管平滑肌细胞（VSMC）增殖以及内皮素-1（ET-1）刺激的ET(A)受体mRNA表达的影响。建立了ET-1诱导培养的大鼠主动脉平滑肌细胞增殖的实验模型。本研究采用3H-胸腺嘧啶核苷（[3H]-TdR）掺入法、细胞计数法和逆转录-聚合酶链反应（RT-PCR）。
选择性ET(A)受体拮抗剂BQ123抑制了VSMC对ET-1反应时[3H]-TdR掺入量和细胞数量的增加。17β-雌二醇可逆转ET-1刺激引起的[3H] TdR掺入量和细胞数量的增加。17β-雌二醇下调ET(A)受体mRNA表达，在12小时时达到最大，雌激素受体拮抗剂他莫昔芬可部分阻断这种下调。
ET-1刺激的VSMC增殖主要通过ET(A)受体。17β-雌二醇抑制ET-1刺激的VSMC增殖，这可能是通过下调ET(A)受体实现的。
