| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 1931020 | Biochemical and Biophysical Research Communications | 2011 | 5 Pages |
It was previously shown that 14-3-3η is overexpressed in the synovial fluid of patients with joint inflammation, which is often associated with growth failure. In this study, we investigated the role of 14-3-3η in chondrogenesis using ATDC5 cells. Upon treatment with TNF-α, cells overexpressed 14-3-3η with inhibition of chondrogenesis. Chondrogenesis was also inhibited by overexpression of 14-3-3η without TNF-α treatment, whereas silencing of 14-3-3η promoted chondrogenic differentiation. Further, G1 phase arrest was inhibited by overexpression of 14-3-3η. In summary, we suggest that 14-3-3η plays a regulatory role in chondrogenic differentiation.
Research highlights► Upon treatment with TNF-α, cells overexpressed 14-3-3η with inhibition of chondrogenesis. ► Chondrogenesis was also inhibited by overexpression of 14-3-3η without TNF-α treatment. ► Silencing of 14-3-3η promoted chondrogenic differentiation. ► G1 phase arrest was inhibited by overexpression of 14-3-3η. ► In summary, we suggest that 14-3-3η plays a regulatory role in chondrogenic differentiation.
