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Lin28a overexpression reveals the role of Erk signaling in articular cartilage development.

Tatsuya KobayashiAnastasia Kozlova
Published in: Development (Cambridge, England) (2018)
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.
Keyphrases
  • cell proliferation
  • signaling pathway
  • pi k akt
  • transcription factor
  • optical coherence tomography
  • type diabetes
  • wild type
  • body composition