VEGF signaling is disrupted in the hearts of mice lacking estrogen receptor alpha

European Journal of Pharmacology
Subrina JesminHiroyuki Kobayashi

Abstract

Estrogen has widely been credited for cardioprotection in women. However, the exact mechanisms that underlie these beneficial estrogenic effects are not completely understood. Here, we sought to: 1) elucidate estrogen's influence on levels of vascular endothelial growth factor (VEGF), a key regulator of cardiovascular processes, and components of its basic signaling machinery (VEGF receptors, Akt, and eNOS) in the heart, and 2) delineate the specific estrogen receptor signaling pathway that mediates its beneficial effects using mice lacking either estrogen receptor alpha or estrogen receptor beta. We analyzed pattern of VEGF signaling and the associated coronary capillary density in the hearts of wild-type (WT), estrogen receptor alpha knockout (ERalpha-KO), and estrogen receptor beta knockout (ERbeta-KO) female mice. Deletion of estrogen receptor alpha causes a marked decrease in coronary capillary density compared to wild-type (WT) mice, while that of estrogen receptor beta had a minimal effect. Consistent with reduced coronary capillary density, cardiac expression levels of VEGF and its signaling molecules (two receptors, phosphorylated Akt, and eNOS) in ERalpha-KO mice were reduced to half of WT, in contrast to ERbeta-KO mi...Continue Reading

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Citations

Jun 1, 2012·Archives of Toxicology·Katherine A Burns, Kenneth S Korach
Apr 10, 2012·Pharmacology & Therapeutics·A A Knowlton, A R Lee
Mar 7, 2014·Journal of Zhejiang University. Science. B·Jie DingXiao-gang Guo
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