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Open AccessArticle

Galectin 3 Deficiency Alters Chondrocyte Primary Cilium Formation and Exacerbates Cartilage Destruction via Mitochondrial Apoptosis

1
Université de Paris, BIOSCAR UMR 1132, Inserm, F-75010 Paris, France
2
UMR 7592 CNRS, Institut Jacques Monod, Univ. Paris Diderot, Sorbonne Paris Cité, F-75205 Paris, France
3
UMR 7365, CNRS-Université de Lorraine, IMoPA, F-54000 Vandœuvre-lés-Nancy, France
4
Rheumatology Research and Advanced Therapeutics, Department of Rheumatology, Radboud University Medical Centre, 6500 HB Nijmegen, The Netherlands
5
Service de Rhumatologie, Centre Viggo Petersen, AP-HP, hôpital Lariboisière, F-75010 Paris, France
*
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Int. J. Mol. Sci. 2020, 21(4), 1486; https://doi.org/10.3390/ijms21041486
Received: 21 December 2019 / Revised: 24 December 2019 / Accepted: 20 February 2020 / Published: 22 February 2020
(This article belongs to the Special Issue Molecular Processes in Chondrocyte Biology)
Mechanical overload and aging are the main risk factors of osteoarthritis (OA). Galectin 3 (GAL3) is important in the formation of primary cilia, organelles that are able to sense mechanical stress. The objectives were to evaluate the role of GAL3 in chondrocyte primary cilium formation and in OA in mice. Chondrocyte primary cilium was detected in vitro by confocal microscopy. OA was induced by aging and partial meniscectomy of wild-type (WT) and Gal3-null 129SvEV mice (Gal3−/−). Primary chondrocytes were isolated from joints of new-born mice. Chondrocyte apoptosis was assessed by Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL), caspase 3 activity and cytochrome c release. Gene expression was assessed by qRT-PCR. GAL3 was localized at the basal body of the chondrocyte primary cilium. Primary cilia of Gal3−/− chondrocytes were frequently abnormal and misshapen. Deletion of Gal3 triggered premature OA during aging and exacerbated joint instability-induced OA. In both aging and surgery-induced OA cartilage, levels of chondrocyte catabolism and hypertrophy markers and apoptosis were more severe in Gal3−/− than WT samples. In vitro, Gal3 knockout favored chondrocyte apoptosis via the mitochondrial pathway. GAL3 is a key regulator of cartilage homeostasis and chondrocyte primary cilium formation in mice. Gal3 deletion promotes OA development. View Full-Text
Keywords: Galectin 3; primary cilium; chondrocyte; osteoarthritis; mechanical stress; apoptosis Galectin 3; primary cilium; chondrocyte; osteoarthritis; mechanical stress; apoptosis
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MDPI and ACS Style

Hafsia, N.; Forien, M.; Renaudin, F.; Delacour, D.; Reboul, P.; Van Lent, P.; Cohen-Solal, M.; Lioté, F.; Poirier, F.; Ea, H.K. Galectin 3 Deficiency Alters Chondrocyte Primary Cilium Formation and Exacerbates Cartilage Destruction via Mitochondrial Apoptosis. Int. J. Mol. Sci. 2020, 21, 1486.

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