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Sost deficiency led to a greater cortical bone formation response to mechanical loading and altered gene expression
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Study demonstrated that sclerostin is expressed in chondrocytes and upregulates the early stage of chondrogenic differentiation in vitro. Furthermore, sclerostin downregulates the expression of markers associated with the late stage of chondrogenic differentiation.
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Oxygen sensing by PHD2 in osteocytes negatively regulates bone mass through epigenetic regulation of sclerostin and targeting PHD2 elicits an osteo-anabolic response in osteoporotic mouse models.
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Findings establish mechanical loading-induced attenuation of sclerostin expression and elevation of bone formation along the subchondral bone plate surface as the major mechanisms characterizing subchondral bone phenotypes associated with severe late-stage osteoarthritis in mice
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The SOST gene inhibited the expression of COL1, OCN, and OPN, reduced the activity of alkaline phosphatase, and increased the expression of LPL and PPARgamma.
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Since adipocytes do not produce sclerostin, these findings suggest an unexplored endocrine function for sclerostin that facilitates communication between the skeleton and adipose tissue.
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A microtubule-dependent mechanotransduction pathway that linked fluid shear stress to reactive oxygen species and calcium (Ca2+) signals that led to a reduction in sclerostin abundance in cultured osteocytes.
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osteoclast-derived LIF regulates bone turnover through sclerostin expression.
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our study provided histological evidences that sclerostin tends to be secreted in osteocytes of remodeled mature bone, while FGF23 would be differently synthesized in osteoblasts and osteocytes according to the developmental stages
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These results show that osteocytes and/or osteoblasts secrete factors regulating beige adipogenesis, at least in part, through the Wnt-signaling inhibitor sclerostin.
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In vivo muCT analysis of cortical bone at age 1 and 3 months confirmed increased thickness in Sost-/-mice, but revealed no cortical abnormalities in single Gja1+/-or Sost+/-mice
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loss of BMP signaling specifically in osteocytes dramatically increases bone mass presumably through simultaneous inhibition of RANKL and SOST, leading to osteoclast inhibition and Wnt activation together.
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humanized Multiple Myeloma xenograft mouse model bearing human MM cells (NOD-SCID.CB17 male mice injected intravenously with 2.5 million of MM1.S-Luc-GFP cells) demonstrated significantly higher concentrations of mouse-derived sclerostin, suggesting a microenvironmental source of sclerostin.
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Protection From Glucocorticoid-Induced Osteoporosis by Anti-Catabolic Signaling in the Absence of Sost/Sclerostin
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Osteocyte-derived molecule sclerostin drives bone marrow adipogenesis.
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complete absence of sclerostin has only minor effects on chronic kidney disease-induced bone loss in mice.
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In mice, sclerostin deficiency hastened reparative dentinogenesis after pulp injury, suggesting that the inhibition of sclerostin may constitute a promising therapeutic strategy for improving the healing of damaged pulps.
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These data suggest that sclerostin plays an important role in the bone remodeling of tooth movement.
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Sclerostin inhibits angiotensin II-induced aortic aneurysm and atherosclerosis via wnt signaling pathway inhibition.
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Analysis of SOST expression using large minigenes reveals the MEF2C binding site in the evolutionarily conserved region (ECR5) enhancer mediates forskolin, but not 1,25-dihydroxyvitamin D3 or TGFbeta1 responsiveness.
