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IGF‐1 and Ang II regulate expression of the G protein‐coupled estrogen receptor in vascular smooth muscle cells.
Author(s) -
Duong Jennifer Lee,
Lindsey Sarah H
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.826.3
Subject(s) - gper , endocrinology , medicine , vascular smooth muscle , estrogen receptor , estrogen , angiotensin ii , receptor , biology , ovariectomized rat , smooth muscle , cancer , breast cancer
Young premenopausal females have a lower incidence of many cardiovascular diseases compared to males, but this protection significantly declines with aging and menopause. We have previously shown that the G protein‐coupled estrogen receptor (GPER) mediates many beneficial effects of estrogen in the cardiovascular system. In addition, GPER expression and function is decreased in the vasculature of aging rats and mice. The goal of the current study was to identify a mechanism by which aging decreases vascular GPER expression. Since circulating levels of angiotensin II (Ang II) and IGF‐1 are altered with aging, we assessed the impact of these two factors on GPER expression in vitro . We hypothesized that IGF‐1 signaling would positively influence GPER expression, while Ang II would negatively regulate GPER. A7r5 cells, an embryonic rat aortic smooth muscle cell line, were exposed to Ang II (100 nM) or IGF‐1 (100 ng/ml) for 24h before cells were harvested and GPER protein was assessed by immunoblot. In comparison to our previous work with primary cultured vascular smooth muscle cells, GPER expression in A7r5 cells was stable throughout passaging. Treatment with IGF‐1 significantly increased GPER expression (0.34 ± 0.05 vs. 1.37 ± 0.14 P<0.05 n=2–3) Conversely, Ang II treatment significantly repressed the expression of GPER (1.04 ± 0.06 vs. 0.83 ± 0.01 P<0.05 n=3). Thus, we conclude that aging‐induced decreases in IGF‐1 signalling and/or increases in Ang II that occur with aging or cardiovascular disease may influence GPER expression. We propose that loss of GPER signalling will diminish the cardiovascular protective effects of estrogen in aging postmenopausal women.