Zinc finger protein 467 regulates Wnt signaling by modulating the expression of sclerostin in adipose derived stem cells.
You L., Chen L., Pan L., Gu WS., Chen JY.
Animal Study, published in Biochem Biophys Res Commun (2014) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- Biochem Biophys Res Commun (2014)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 25490389
- DOI
- 10.1016/j.bbrc.2014.11.120
- Citations
- 15
Abstract (original English)
Osteoporosis is a metabolic disease in which a disruption of the balance between bone formation by osteoblasts and bone resorption by osteoclasts leads to the progressive deterioration of bone density and quality. Tissue engineering approaches to the treatment of osteoporosis depend on the identification of factors that promote the differentiation of progenitor cells towards an osteoblastic phenotype. In the present study, we expanded on prior findings on the role of zinc finger protein 467 (Zfp467) in the osteoblastic differentiation of adipose-derived stem cells (ADSCs) and explored the underlying mechanisms. We showed that Zfp467 binds to and regulates the expression of the SOST gene, which encodes a secreted glycoprotein named sclerostin (Sost) that is expressed exclusively by osteocytes and functions as a negative regulator of bone formation through the modulation of Wnt signaling. Overexpression of Zfp467 in ADSCs inhibited Wnt signaling by promoting binding of Sost to the Wnt coreceptors LRP5/6 and disrupting Wnt induced Frizzled-LRP6 complex formation, and siRNA mediated Sost silencing reversed the inhibition of Wnt signaling by Zfp467 in ADSCs. Our results indicate that Zfp467 regulates the differentiation of ADSCs via a mechanism involving Sost-mediated inhibition of Wnt signaling, suggesting potential therapeutic targets for the treatment of osteoporosis.
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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