Mechanical stretch inhibits myoblast-to-adipocyte differentiation through Wnt signaling
Biochemical and Biophysical Research Communications, ISSN: 0006-291X, Vol: 329, Issue: 1, Page: 381-385
2005
- 61Citations
- 57Captures
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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.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations61
- Citation Indexes61
- 61
- CrossRef58
- Captures57
- Readers57
- 57
Article Description
Myoblasts are able to differentiate into other mesenchymal lineages including adipocytes and osteoblasts. However, it is not known how this differentiation is normally regulated in intact animals and humans. Here, we subjected cultured C2C12 myoblasts to cyclic mechanical stretch (20% elongation) during differentiation into adipocytes. Mechanical stretch inhibited the myoblast-to-adipocyte differentiation significantly, concurrent with an enhanced expression of Wnt10b mRNA. Inhibition of the Wnt signaling by incubation of the myoblasts with a soluble Wnt ligand, sFRP-2, abolished the inhibitory function of mechanical stretch on adipogenesis. These findings provide evidence that mechanical stretch inhibits myoblast-to-adipocyte differentiation possibly through Wnt signaling.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0006291X05001221; http://dx.doi.org/10.1016/j.bbrc.2005.01.136; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=13844281666&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/15721317; https://linkinghub.elsevier.com/retrieve/pii/S0006291X05001221; https://dx.doi.org/10.1016/j.bbrc.2005.01.136
Elsevier BV
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