一氧化氮选择性抑制17β-雌二醇诱导的基因表达，而不影响HeLa细胞中的非基因组事件。

Nitric oxide inhibits selectively the 17beta-estradiol-induced gene expression without affecting nongenomic events in HeLa cells.

作者信息

Marino M, Ficca R, Ascenzi P, Trentalance A

机构信息

Department of Biology, University "Roma Tre,", Viale G. Marconi 446, Rome, I-00146, Italy.

出版信息

Biochem Biophys Res Commun. 2001 Aug 24;286(3):529-33. doi: 10.1006/bbrc.2001.5433.

DOI:10.1006/bbrc.2001.5433

PMID:11511091

Abstract

17beta-Estradiol (E2) induces genomic (i.e., pC3-luciferase promoter-reporter construct expression) and nongenomic (i.e., DNA synthesis and IP(3) production) effects in HeLa cells only after transient transfection with the human estrogen receptor alpha (ERalpha) reporter plasmid. Here the effect of nitric oxide (NO) on both E2-induced effects in transiently transfected HeLa cells is reported. Remarkably, the E2-dependent gene transcription is inhibited dose-dependently by NO. By contrast, DNA synthesis and IP(3) production, representing nongenomic E2-dependent effects, are unaffected by NO. The selective NO action on E2-induced functions may be related to NO-mediated chemical modification(s) of the Cys residues present in the DNA recognition domain of ERalpha impairing DNA binding.

摘要

仅在用人雌激素受体α（ERα）报告质粒瞬时转染HeLa细胞后，17β-雌二醇（E2）才会在HeLa细胞中诱导基因组效应（即pC3-荧光素酶启动子-报告基因构建体表达）和非基因组效应（即DNA合成和IP(3)产生）。本文报道了一氧化氮（NO）对瞬时转染的HeLa细胞中E2诱导的两种效应的影响。值得注意的是，E2依赖性基因转录受到NO的剂量依赖性抑制。相比之下，代表非基因组E2依赖性效应的DNA合成和IP(3)产生不受NO影响。NO对E2诱导功能的选择性作用可能与NO介导的ERα DNA识别域中存在的半胱氨酸残基的化学修饰损害DNA结合有关。