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Estrogen's actions transcend a sole reproductory function in cell signaling.

A literature has been emerging showing that estrogen exhibits functions that transcends its role in reproduction. 17beta-estradiol stimulates nitric oxide (NO) release from human internal thoracic artery fragments and from cultured arterial endothelial cells by acting on an estrogen cell surface receptor. Estrogen down regulates immunocyte functions, i.e. chemotaxis and phagocytosis, as well. Monocytes express estrogen receptor mRNA as well as an estrogen receptor binding site. Importantly, estrogen exerts non reproductive roles in invertebrates. These reports also demonstrate that invertebrate estrogen receptors are coupled to constitutive NO release and are located on the cell surface, suggesting they first appear very early in evolution. All in all, estrogen's ability to stimulate constitutive nitric oxide synthase derived NO is significant since NO is also considered an important inhibitory agent that diminishes immunocyte adhesion and the vascular endothelium's capability to adhere immunocytes, as well as down regulating various immunocytes both before and after proinflammatory events. These findings promise to open up new areas of investigation concerning estrogen associated biomedical phenomena, including cellular protection processes.