Functional interaction between Wnt and Bmp signaling in periosteal bone growth
Scientific Reports, ISSN: 2045-2322, Vol: 11, Issue: 1, Page: 10782
2021
- 14Citations
- 49Usage
- 10Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations14
- Citation Indexes14
- 14
- CrossRef3
- Usage49
- Downloads45
- Abstract Views4
- Captures10
- Readers10
- 10
Article Description
Wnt and Bmp proteins are well known to regulate bone development and homeostasis. Although both signals are extensively studied, their potential interaction in vivo is less well understood. Previous studies have shown that deletion of Bmpr1a, a type I receptor for Bmp signaling, results in excessive trabecular bone formation while diminishing periosteal bone growth. Moreover, forced-expression of the Wnt antagonist Sost suppresses the overgrowth of trabecular bone caused by Bmpr1a deletion, thus implicating hyperactive Wnt signaling in the excessive trabecular bone formation. However, it remains uncertain whether Wnt and Bmp signaling interacts in regulating the periosteal bone growth. Here we show that multiple Wnt genes are markedly suppressed in the cortical bone without Bmpr1a. Importantly, overexpression of Wnt7b fully rescues periosteal bone growth in the Bmpr1a-deficient mice. Thus, pharmacological activation of Wnt signaling can restore normal bone size without intact Bmp signaling.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85106645788&origin=inward; http://dx.doi.org/10.1038/s41598-021-90324-1; http://www.ncbi.nlm.nih.gov/pubmed/34031510; https://www.nature.com/articles/s41598-021-90324-1; https://digitalcommons.wustl.edu/open_access_pubs/10407; https://digitalcommons.wustl.edu/cgi/viewcontent.cgi?article=11405&context=open_access_pubs; https://dx.doi.org/10.1038/s41598-021-90324-1
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