Department of Experimental Medical Science, Lund University, Lund, Sweden.
Mol Cell Endocrinol. 2010 May 5;319(1-2):8-13. doi: 10.1016/j.mce.2010.01.002. Epub 2010 Jan 13.
Endothelial cells express both estrogen receptor (ER) alpha and beta. The objective of this study was to investigate if and how mediators of inflammation regulate endothelial cell ERalpha and ERbeta expression. ERalpha and ERbeta transcript and protein expression were determined by real-time quantitative PCR and Western blotting, respectively, in endothelial cell line bEnd.3 cells stimulated with the inflammation promoter lipopolysaccharide (E. coli LPS). Stimulation with LPS (500 ng/ml and 10 microg/ml) for 4 days reduced both ERalpha and ERbeta mRNA levels. The glucocorticoid dexamethasone (1 microM) had no effect on LPS-induced attenuation of ERalpha and beta transcript expression. Full-length 66-67 kDa ERalpha protein was unaffected by 4 days stimulation with LPS, while the 46-kDa ERalpha isoform was reduced by about 20%. ERbeta protein was reduced by about 40% by LPS at 4 days. Treatment with 17beta-estradiol (E(2), 100 nM) for 4 days increased ERbeta mRNA by about 8 times but had no effect on ERalpha mRNA level. The E(2)-induced increase in ERbeta transcript was not associated with increased ERbeta protein. E(2) increased ERbeta mRNA expression also in the presence of LPS, suggesting that inflammation-induced impairment of ERbeta signalling is rescued by estrogen.
内皮细胞表达雌激素受体 (ER)α和β。本研究旨在探讨炎症介质是否以及如何调节内皮细胞 ERα和 ERβ的表达。通过实时定量 PCR 和 Western blot 分别确定内皮细胞系 bEnd.3 细胞在炎症启动子脂多糖 (大肠杆菌 LPS)刺激下 ERα和 ERβ的转录本和蛋白表达。用 LPS (500ng/ml 和 10μg/ml)刺激 4 天可降低 ERα和 ERβ mRNA 水平。糖皮质激素地塞米松 (1μM)对 LPS 诱导的 ERα和β转录表达衰减没有影响。全长 66-67 kDa ERα蛋白不受 LPS 刺激 4 天的影响，而 46 kDa ERα同工型减少约 20%。LPS 在 4 天时将 ERβ蛋白减少约 40%。用 17β-雌二醇 (E2，100 nM)处理 4 天可使 ERβ mRNA 增加约 8 倍，但对 ERα mRNA 水平没有影响。E2 诱导的 ERβ转录本增加与 ERβ蛋白增加无关。E2 也可在 LPS 存在的情况下增加 ERβ mRNA 表达，表明雌激素可挽救炎症诱导的 ERβ信号受损。
