Estrogen down-regulates nicotine-induced adhesion molecule expression via nongenomic signal pathway in endothelial cells

International Immunopharmacology
Yajing WangZhongdong Qiao

Abstract

Although gonadal hormone mostly causes genotropic actions through the members of nuclear receptor family, it also can regulate these actions via membrane receptor. To explore the possibility of plasma membrane estrogen receptors (mER) mediating genotropic events, we have investigated estrogen's effect on nicotine-stimulated adhesion molecule expression and evaluated whether this effect depends on calcium, MAPK signal pathway. Fluorescence Spectroscopy analysis of Ca2+ from human umbilical vein endothelial cells (HUVECs) showed through mER, estrogen induced a rapid rise of intracellular free Ca2+ concentration and this rise could not be inhibited by tamoxifen (classic ER inhibitor). In the context of nicotine stimulating, however, estrogen attenuated phosphorylation of mitogen-activated protein kinase (MAPK) family members, extracellular signal regulated kinase 1/2 (ERK1/2), p38 but not c-Jun-N-terminal kinase (JNK) in HUVECs and this effect could not still be prevented by tamoxifen. In the meantime, estrogen also down-regulated surface/soluble vascular cell adhesion molecule (VCAM-1, sVCAM-1) and endothelial selectin (E-selectin, sE-selectin) levels, which was not abolished by tamoxifen either. Moreover, calcium chelator BAPTA,...Continue Reading

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Citations

Mar 12, 2011·American Journal of Orthodontics and Dentofacial Orthopedics : Official Publication of the American Association of Orthodontists, Its Constituent Societies, and the American Board of Orthodontics·Ahmad SodagarMohammad Javad Kharrazifard
Jan 29, 2011·Brain Research Bulletin·Gorkem Yararbas, Sakire Pogun
Dec 10, 2008·Pharmacology & Therapeutics·Richard D EgletonPiyali Dasgupta
Jul 12, 2008·IUBMB Life·Xiao-Dong Fu, Tommaso Simoncini
Jan 31, 2007·Annals of the New York Academy of Sciences·Mariam Klouche

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