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KMID : 0358420110540090499
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Korean Journal of Obstetrics and Gynecology
2011 Volume.54 No. 9 p.499 ~ p.507
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The effect of estrogen on extracellular signal-regulated kinases activation in uterine artery smooth muscle cells during pregnancy
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Lee Yong-Woo
Kim Ho-Yeon
Park Sang-Min
Choi Su-Ran
Chung Ji-Youn
Moon Chong-Soo
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Abstract
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Objective :To explore the endothelium-independent mechanisms of estrogen induced uterine vasodilatation, this study was performed to determine whether uterine artery smooth muscle (UASM) cells are direct targets of estrogen, and estradiol (E2) stimulates extracellular signal-regulated kinases (ERK2/1) in endothelium denuded UASMs.
Methods:The uterine arteries were obtained from late gestation pregnant sheep and the endothelium was denuded with collagenase digestion. The uterine artery smooth muscle segments were digested, collected and cultured. Endothelial integrity and smooth muscle status were assessed by Double immunofluorescence staining and flow cytometry. The UASM cells were treated with increasing concentrations of E2 (10-14 to 10-6 M), and pretreated with ICI 182,780 followed by different concentrations (10-10 and 10-7 M) of E2. Western blot analysis of ERK2/1 phosphorylation with a phospho-mitogen activated protein kinases (MAPKs) antibody were carried out to total cell extracts.
Results:The loss of endothelial function and adequacy of smooth muscle integrity were confirmed. When challenged with increasing concentrations of E2, a bi-phase ERK2/1 phosphorylation was observed. Treatment with low doses (10-14 to 10-10 M) of E2, ERK2/1 phosphorylation was dose-dependently increased, whereas high doses (10-9 to 10-8 M) did not phosphorylate ERK2/1. However, treatment with pharmacological doses (10-7 to 10-6 M) drastically phosphorylated ERK2/1. In the presence of ICI 182,780, E2 induced ERK2/1 phosphorylation were abolished in both.
Conclusion:It suggests that UASM is the target tissue of estrogen during uterine vasodilatation, and estrogen stimulation of ERK2/1 activation is mediated by an estrogen receptor-dependent mechanism. It also is presumed that endothelium independent mechanism exists in estrogen induced vasodilatation.
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KEYWORD
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Estrogen, Uterine artery smooth muscle, Vasodilatation, ERK2/1
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