期刊
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
卷 23, 期 2, 页码 198-203出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/01.ATV.0000053846.71621.93
关键词
estrogen; estrogen receptor; nontranscriptional signaling; phosphatidylinositol 3-kinase; endothelium
资金
- NHLBI NIH HHS [HL70274, HL48743, HL52233] Funding Source: Medline
Objective-Nontranscriptional signaling mechanisms mediate some of the biological effects of estrogen, such as the rapid actions on the blood vessels. By interacting with phosphatidylinositol 3-kinase (PI3K), estrogen receptor (ER) alpha leads to activation of protein kinase Akt and to subsequent increase in endothelial nitric oxide synthase activity. Because PI3K is mainly a cytoplasmic complex, we studied the cellular site of interaction between this enzyme and ERalpha, and we dissected the molecular mechanisms that mediate this interaction. Methods and Results-By using cultured human saphenous vain endothelial cells, we found that cell membrane-bound ERalpha colocalizes with PI3K and may be responsible for PI3K activation. Furthermore, we characterized the subsequent steps in the activation of the PI3K/Akt signaling cascade, comparing the molecular events that follow insulin or estradiol activation of PI3K. Conclusions-We provide novel evidence for an important role of nonnuclear estrogen receptor in rapid, nontranscriptional responses of human endothelial cells to estrogen.
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