Restriction of spontaneous and prednisolone-induced leptin production to dedifferentiated state in human hip OA chondrocytes: role of Smad1 and β-catenin activation

Osteoarthritis and Cartilage
Edith CharlierMichel G Malaise

Abstract

The aetiology of OA is not fully understood although several adipokines such as leptin are known mediators of disease progression. Since leptin levels were increased in synovial fluid compared to serum in OA patients, it was suggested that joint cells themselves could produce leptin. However, exact mechanisms underlying leptin production by chondrocytes are poorly understood. Nevertheless, prednisolone, although displaying powerful anti-inflammatory properties has been recently reported to be potent stimulator of leptin and its receptor in OA synovial fibroblasts. Therefore, we investigated, in vitro, spontaneous and prednisolone-induced leptin production in OA chondrocytes, focusing on transforming growth factor-β (TGFβ) and Wnt/β-catenin pathways. We used an in vitro dedifferentiation model, comparing human freshly isolated hip OA chondrocytes cultivated in monolayer during 1 day (type II, COL2A1 +; type X, COL10A1 + and type I collagen, COL1A1 -) or 14 days (COL2A1 -; COL10A1 - and COL1A1+). Leptin expression was not detected in day1 OA chondrocytes whereas day14 OA chondrocytes produced leptin, significantly increased with prednisolone. Activin receptor-like kinase 1 (ALK1)/ALK5 ratio was shifted during dedifferentiation, f...Continue Reading

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Citations

Dec 22, 2016·International Journal of Molecular Sciences·Edith CharlierDominique De Seny
Nov 30, 2019·Evidence-based Complementary and Alternative Medicine : ECAM·Mustapha Zeddou
Feb 6, 2019·Cell Death & Disease·Céline DeroyerDominique de Seny
Oct 13, 2019·Developmental Biology·Samir A BelloJosé E García-Arrarás

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