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Follicle Stimulating Hormone Stimulation of a Murine Monocyte Cell Line
Author(s) -
Leamon Annie B.,
Cohen Brian D.
Publication year - 2018
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.2018.32.1_supplement.533.64
Subject(s) - rankl , creb , osteoclast , follicle stimulating hormone , medicine , endocrinology , estrogen , osteoporosis , follicle stimulating hormone receptor , monocyte , hormone , chemistry , microbiology and biotechnology , biology , transcription factor , luteinizing hormone , activator (genetics) , receptor , gene , biochemistry
Osteoporosis, an illness resulting in weak and brittle bones, will soon cause over $25 billion dollars of economic damage to the US economy each year. For decades, menopausal osteoporosis was thought to be the result of estrogen loss due to depletion of ovarian follicles. Recent research, however, has shown that the hormone primarily responsible for estrogen synthesis, follicle stimulating hormone (FSH), can contribute to bone degeneration. What is unclear is the specific mechanism by which FSH has this effect. We hypothesized that FSH may contribute to monocyte differentiation to osteoclasts. To test this, we used the RAW 246.7 murine monocyte cell line which can differentiate into osteoclasts in the presence of RANKL. We were able to find evidence of FSH‐dependent signaling in cells FSH treated cells with or without RANKL. In particular, time dependent activation of the cyclic AMP Response Element Binding Protein (CREB) was observed. Interestingly, RANKL treatment changed the pattern of phosphorylation of CREB and the related transcription factor ATF1. Since CREB partially regulates osteoclast differentiation and function this could be one part of the mechanism by which FSH stimulates osteoclastogenesis and bone demineralization. With this in mind, future therapies targeting FSH action could be developed to prevent the onset of osteoporosis. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .