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Effects of 17 β-estradiol on lipopolysacharride-induced intracellular adhesion molecule-1 mRNA expression and Ca²+ homeostasis alteration in human endothelial cells.

Abstract：

:Recent evidence showed that 17 β-estradiol (E₂) decreased cytokine-induced expression of cell adhesion molecules (CAM). Changes in intracellular Ca²+ concentration ([Ca²+](i)) has been shown to be associated with CAM expression in endothelial cells. Here, the effects of E₂ (1 μM, 24 h) on the expression of intracellular adhesion molecule-1 (ICAM-1) and [Ca²+](i) were investigated in a lipopolysaccharide (LPS) (100 ng/mL, 18 h)-stimulated human endothelial cell line, EA.hy926, using real-time PCR and spectrofluorometry, respectively. PCR analysis revealed a significant increase in ICAM-1 expression in calcium ionophore A23187 (1 nM)- or LPS-stimulated cells. Pretreatment of cells with E(2) significantly inhibited LPS-induced ICAM-1 mRNA expression. [Ca²+](i) was monitored in Fura-2AM-loaded cells in the presence and absence of extracellular Ca²+ with thapsigargin (TG, 1 μM), a sarco/endoplasmic reticulum ATPase inhibitor or ATP (100 μM). The extent of TG- or ATP-induced [Ca²+](i) increase was significantly higher in LPS-stimulated cells than in control cells. Pre-treatment of LPS-stimulated cells with E₂ limited the Ca²+ response to the same level as in control cells. Furthermore, ICI 182,780, an estrogen receptor antagonist, attenuated the inhibitory actions of E₂ on ICAM-1 mRNA expression and Ca²+ responses, suggesting that estrogen receptors mediate, at least in part, the effects of estrogen. These data suggest a potential underlying mechanism for the protective effect of E₂ against atherosclerosis.

journal_name

Vascul Pharmacol

journal_title

Vascular pharmacology

authors

Thor D,Zhang R,Anderson L,Bose DD,Dubé GP,Rahimian R

doi

10.1016/j.vph.2010.09.001

subject

Has Abstract

pub_date

2010-11-01 00:00:00

pages

230-8

issue

5-6

eissn

1537-1891

issn

1879-3649

pii

S1537-1891(10)00129-1

journal_volume

53

pub_type

杂志文章

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