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

BioMed Research International - Tập 2017 - Trang 1-12 - 2017
David Moulin1, Véronique Salone1, Meriem Koufany1, Thomas Clément1, Isabelle Behm‐Ansmant1, Christiane Branlant1, Bruno Charpentier1, Jean‐Yves Jouzeau2,1
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

Tóm tắt

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 inin vitromodels of chondrocyte phenotype changes (IL-1βchallenge or serial subculturing) and in chondrocytes from OA and non-OA patients. Potential miR-29b targets identifiedin silicoin 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.

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BioMed Research International

Tập 2017

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