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Statins do not inhibit the FGFR signaling in chondrocytes

B Fafilek1, M Hampl2, N Ricankova3

  • 1Department of Biology, Faculty of Medicine, Masaryk University, 62500, Brno, Czech Republic; International Clinical Research Center, St. Anne's University Hospital, 65691, Brno, Czech Republic.

Osteoarthritis and Cartilage
|June 7, 2017
PubMed
Abstract

Insights

Statins do not inhibit fibroblast growth factor receptor 3 (FGFR3) signaling in chondrocytes. This suggests statin benefits for FGFR3-related chondrodysplasia may not originate within growth plate cartilage.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Genetics

Background:

  • Statins, cholesterol-lowering drugs, may counteract aberrant fibroblast growth factor receptor 3 (FGFR3) signaling.
  • FGFR3 mutations cause human dwarfing conditions, presenting a potential therapeutic target for statins.
  • The mechanism of statin action on FGFR3 signaling remains unclear.

Purpose of the Study:

  • To investigate the effect of statins on FGFR signaling in chondrocytes.
  • To determine if statins can inhibit FGFR3-mediated effects in cartilage cells.

Main Methods:

  • Primary chondrocytes, mouse embryonic tibia, and limb bud micromasses were treated with FGF2 to activate FGFR signaling.
  • The effects of four statins (atorvastatin, fluvastatin, lovastatin, pravastatin) were evaluated.
  • Assessed FGFR3 protein stability and FGFR-mediated chondrocyte growth arrest, ECM loss, senescence, and differentiation.

Main Results:

  • Statins did not alter FGFR3 protein expression levels.
  • No statin treatment affected FGFR-mediated inhibition of chondrocyte proliferation.
  • Statins did not impact FGFR-mediated hypertrophic differentiation in any model system.

Conclusions:

  • Statins do not inhibit FGFR signaling within chondrocytes.
  • The previously observed statin-mediated rescue of FGFR3-related chondrodysplasia is unlikely to be an intrinsic effect of the growth plate cartilage.
  • Further research is needed to elucidate the mechanism behind statin's therapeutic effects in chondrodysplasia models.
Keywords:
AchondroplasiaChondrocytesFGF signalingStatins

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