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RORβ modulates a gene program that is protective against articular cartilage damage

Mi Ra Chang1, Patrick R Griffin1

  • 1Department of Molecular Medicine, UF Scripps Biomedical Research, University of Florida, Jupiter, FL, United States of America.

Plos One
|October 13, 2022
PubMed

Insights

Osteoarthritis (OA) is a common joint disease. Stable expression of RORβ promotes chondrogenesis and protects against OA by altering FGF receptor signaling and MAPK/AKT pathways.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Orthopedics

Background:

  • Osteoarthritis (OA) is the most common chronic joint disease, affecting over 65s and causing disability.
  • Current OA treatments primarily manage pain and swelling, lacking disease-modifying capabilities.
  • The precise pathogenesis of OA and effective cartilage protection strategies remain elusive.

Purpose of the Study:

  • To investigate the role of RORβ in chondrogenesis and OA development.
  • To determine how RORβ influences specific gene expression programs related to cartilage health.
  • To explore RORβ's impact on key signaling pathways involved in OA pathogenesis.

Main Methods:

  • Stable expression of RORβ in cultured cells.
  • Analysis of gene expression patterns, focusing on FGF receptors (FGFR1, FGFR3).
  • Assessment of downstream signaling pathways, including ERK1/2-MAPK and AKT.

Main Results:

  • RORβ expression altered gene programs supporting chondrogenesis and OA protection.
  • RORβ modulated the ratio of FGFR1 (cartilage destruction) to FGFR3 (cartilage protection) expression.
  • ERK1/2-MAPK signaling was suppressed, while AKT signaling was enhanced by RORβ.

Conclusions:

  • RORβ plays a critical role in chondrogenesis and cartilage protection.
  • RORβ's influence on FGFR and MAPK/AKT signaling pathways is key to its protective effects.
  • Targeting RORβ expression in chondrocytes may offer novel disease-modifying OA therapies.

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