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Estrogen Stimulates Delayed Mitogen-Activated Protein Kinase Activity in Human Endothelial Cells via an Autocrine Loop That Involves Basic Fibroblast Growth Factor
Author(s) -
Seunghee KimSchulze,
William L. Lowe,
H. William Schnaper
Publication year - 1998
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/01.cir.98.5.413
Subject(s) - medicine , autocrine signalling , mitogen activated protein kinase , protein kinase a , estrogen , fibroblast growth factor receptor 4 , microbiology and biotechnology , basic fibroblast growth factor , endocrinology , fibroblast growth factor , growth factor , kinase , fibroblast growth factor receptor , biology , receptor
Estrogen plays a significant role in protecting premenopausal women from cardiovascular disease. We have found that estradiol augments endothelial cell activities related to vascular healing and that human coronary artery and umbilical vein endothelial cells express estrogen receptors (ERs). Classically, the ER functions as a transcription factor, but the cytoplasmic targets of this genomic effect have not been defined for endothelial cells. In the present study, we examined the potential role of the mitogen-activated protein (MAP) kinases ERK1 and ERK2 as mediators of estrogen action.

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