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BioMed Research International
Volume 2017 (2017), Article ID 9792512, 12 pages
https://doi.org/10.1155/2017/9792512
Research Article

MicroRNA-29b Contributes to Collagens Imbalance in Human Osteoarthritic and Dedifferentiated Articular Chondrocytes

1Laboratoire d’Ingénierie Moléculaire et Physiopathologie Articulaire (IMoPA), UMR 7365 CNRS-Université de Lorraine, Biopôle de l’Université de Lorraine, Campus Biologie-Santé, 9 avenue de la Forêt Haye, BP 20199, 54505 Vandœuvre-lès-Nancy Cedex, France
2Département de Pharmacologie Clinique et Toxicologie, Centre Hospitalier Universitaire, Hôpital Central, 29 avenue du Maréchal de Lattre-de-Tassigny, 54035 Nancy Cedex, France

Correspondence should be addressed to Jean-Yves Jouzeau; rf.eniarrol-vinu@uaezuoj.sevy-naej

Received 24 February 2017; Accepted 24 April 2017; Published 22 May 2017

Academic Editor: Magali Cucchiarini

Copyright © 2017 David Moulin et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Objective. Decreased expression of collagen type II in favour of collagen type I or X is one hallmark of chondrocyte phenotype changes in osteoarthritic (OA) cartilage. MicroRNA- (miR-) 29b was previously shown to target collagens in several tissues. We studied whether it could contribute to collagen imbalance in chondrocytes with an impaired phenotype. Methods. After preliminary microarrays screening, miR-29b levels were measured by RT- quantitative PCR in in vitro models of chondrocyte phenotype changes (IL-1β challenge or serial subculturing) and in chondrocytes from OA and non-OA patients. Potential miR-29b targets identified in silico in 3′-UTRs of collagens mRNAs were tested with luciferase reporter assays. The impact of premiR-29b overexpression in ATDC5 cells was studied on collagen mRNA levels and synthesis (Sirius red staining) during chondrogenesis. Results. MiR-29b level increased significantly in IL-1β-stimulated and weakly in subcultured chondrocytes. A 5.8-fold increase was observed in chondrocytes from OA versus non-OA patients. Reporter assays showed that miR-29b targeted COL2A1 and COL1A2 3′-UTRs although with a variable recovery upon mutation. In ATDC5 cells overexpressing premiR-29b, collagen production was reduced while mRNA levels increased. Conclusions. By acting probably as a posttranscriptional regulator with a different efficacy on COL2A1 and COL1A2 expression, miR-29b can contribute to the collagens imbalance associated with an abnormal chondrocyte phenotype.