| First Author | Kobayashi T | Year | 2018 |
| Journal | Development | Volume | 145 |
| Issue | 15 | PubMed ID | 30042178 |
| Mgi Jnum | J:266580 | Mgi Id | MGI:6220821 |
| Doi | 10.1242/dev.162594 | Citation | Kobayashi T, et al. (2018) Lin28a overexpression reveals the role of Erk signaling in articular cartilage development. Development 145(15):dev162594 |
| abstractText | Adult articular cartilage shows limited tissue turnover, and therefore development of the proper structure of articular cartilage is crucial for life-long joint function. However, the mechanism by which the articular cartilage structure is developmentally regulated is poorly understood. In this study, we show evidence that activation of extracellular signal-regulated kinases (Erk1/2) in articular chondrocyte progenitors during developmental stages control articular cartilage thickness. We found that overexpression of Lin28a, an RNA-binding protein that regulates organismal growth and metabolism, in articular chondrocyte progenitor cells upregulated Erk signaling and increased articular cartilage thickness. Overexpression of a constitutively active Kras mimicked Lin28a overexpression, and inhibition of Erk signaling during embryonic stages normalized the cartilage phenotype of both Kras- and Lin28a-overexpressing mice. These results suggest that articular cartilage thickness is mainly determined during the process of embryonic synovial joint development, which is positively regulated by Erk signaling. |
