Previously, our laboratory identified @entity61250 , encoding @entity61250 ( @entity61250 ), as a positional candidate for a pleiotropic quantitative trait locus affecting femoral size, shape, and biomechanical performance. We hypothesized that @entity15486 ( @entity15486 ) signaling promotes osteogenesis. Exposure of immortalized @entity19 osteoblast (TMOb) cells to big @entity15486 increased mineralization. Following big @entity15486 treatment, we measured the secretion of @entity7424 ( @entity7424 ), @entity26735 ( @entity26735 ), and sclerostin ( @entity12456 ). In each case, big @entity15486 signaling changed secretion in a manner that favored increased osteogenic activity. Treatment with @entity61250 , @entity9937 ( @entity9937 ), or WNT receptor antagonists inhibited the big @entity15486 -mediated increase in mineralization. In the presence of big @entity15486 , message levels of @entity2447 , @entity7424 , @entity26735 , and @entity12456 are uncoupled from protein production, suggesting posttranscriptional regulation. To evaluate the role of big @entity15486 in normal bone physiology, we inhibited @entity9937 signaling during mineralization in the absence of exogenous @entity15486 . @entity9937 blockade reduced mineralization, decreased @entity7424 , and increased @entity26735 and @entity12456 secretion, responses opposite to those induced by exogenous big @entity15486 . Pharmacological and siRNA knockdown to inhibit @entity61250 reduced mineralization and @entity7424 secretion with decreasing @entity26735 and decreasing or stable @entity12456 secretion, suggesting a further, unknown role of @entity61250 in osteoblast maturation. Previously we identified miR 126-3p as a potential @entity15486 -responsive regulator of @entity12456 in @entity19 cells. Overexpression of miR126-3p increased mineralization in TMOb cells and decreased @entity12456 secretion. Osteoblasts express the @entity15486 signaling pathway and @entity15486 signaling is necessary for normal osteoblast differentiation and mineralization, acting through regulation of miRs that target osteogenic molecules.

Endothelin signaling regulates mineralization and posttranscriptionally regulates XXXX in TMOb cells via miR 126-3p.

@entity9937 :: ('13617(Tax:10090)', 'Gene') :: ['EDNRA', 'endothelin receptor A'] @entity2447 :: ('12393(Tax:10090)', 'Gene') :: ['Runx2'] @entity19 :: ('10090', 'Species') :: ['murine', 'mouse'] @entity12456 :: ('74499(Tax:10090)', 'Gene') :: ['Sost', 'SOST'] @entity26735 :: ('13380(Tax:10090)', 'Gene') :: ['Dkk1', 'dickkopf-homolog-1 protein 1', 'DKK1'] @entity61250 :: ('230857(Tax:10090)', 'Gene') :: ['endothelin-converting enzyme-1', 'ECE-1'] @entity7424 :: ('16000(Tax:10090)', 'Gene') :: ['IGF1', 'Igf1', 'insulin-like-growth factor-1'] @entity15486 :: ('13614(Tax:10090)', 'Gene') :: ['ET-1', 'endothelin-1']
@entity12456 :: (74499(Tax:10090),Gene) :: ['SOST']
