sclerostin


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sclerostin

A glycoprotein secreted by osteocytes that has anti-anabolic effects on bone. It has a C-terminal cysteine knot-like (CTCK) domain and sequence similarity to the DAN (differential screening-selected gene aberrative in neuroblastoma) family of bone morphogenetic protein (BMP) antagonists.

Molecular pathology
Sclerostin is misregulated in van Buchem disease, which is characterised by increased bone mass.
References in periodicals archive ?
An akt-dependent increase in canonical wnt signaling and a decrease in sclerostin protein levels are involved in strontium ranelate-induced osteogenic effects in human osteoblasts.
The aim of this study was to assess systemic alterations of DKK-1 and sclerostin in patients with different stages of PC.
Sclerostin was determined by enzyme immunoassay (Biomedica, Vienna, Austria, distributed by Alpco, intra- and interassay CVs 3.7% and 3.7%, respectively).
demonstrated the reduction of tissue expression of sclerostin at entheseal sites and in blood samples of AS patients compared with healthy subjects and patients affected by rheumatoid arthritis [9, 10].
PTH downregulates the expression of Sost, which encodes sclerostin, a potent inhibitor of bone formation mediated by T-cell-produced Wnt10b that is expressed by osteocytes (Bellido et al., 2005; Keller & Kneissel; Li et al., 2014).
They develop increasing osteoproliferation visible as classical syndesmophytes causing fusion of the vertebral bodies identified as "AS with bamboo spine." The risk factors/forces include male gender, socioeconomic factors (including physical stress), environment factors (smoking, others?), genetic factors (HLA B27, certain genotypes, ERAP-1, and IL23R), certain receptor protein biomarkers (KIR3DL1, Sclerostin, and Dkk-1, others?), intensity of acute phase response (genetically determined, CRP, others?), presence of syndesmophyte(s) at first presentation, and other possible factors.
DKK1 and sclerostin have a direct effect on bone formation through interaction with the Wnt signaling pathway [39] but they have not been extensively studied in RA patients under TNFi.
Furthermore, in a secondary analysis in the paricalcitol and endothelial function in chronic kidney disease (PENNY) trial [10], we have recently observed that pentosidine modifies the sclerostin response to VDR activation by paricalcitol [11].
Evidences show that dihydromyricetin decreases the expression of kickkopf-1 and sclerostin and increase [beta]-catenin transcriptional activity, resulting in enhancing osteogenic differentiation in vitro [67].
Romosozumab is a monoclonal antibody that binds sclerostin, increasing bone formation and decreasing bone resorption.
Injecting a Wnt-blocking molecule called sclerostin into degenerated TMJs in animals stimulated cartilage growth and healing of the joint.
As Wnt signaling inhibitors, the expression of Dickkopf (DKK)-1 and sclerostin were reduced in the spine of proteoglycan-induced spondylitis mice (2) and blockade of DKK-1 induces fusion of sacroiliac joints in tumor necrosis factor (TNF) transgenic mice, (3) implicating the Wnt pathway as a likely mediator of the mechanism by which inflammation induces bony ankylosis in spondyloarthritis.