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

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 collage...

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Autores principales: Moulin, David, Salone, Véronique, Koufany, Meriem, Clément, Thomas, Behm-Ansmant, Isabelle, Branlant, Christiane, Charpentier, Bruno, Jouzeau, Jean-Yves
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5458373/
https://www.ncbi.nlm.nih.gov/pubmed/28612031
http://dx.doi.org/10.1155/2017/9792512
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author Moulin, David
Salone, Véronique
Koufany, Meriem
Clément, Thomas
Behm-Ansmant, Isabelle
Branlant, Christiane
Charpentier, Bruno
Jouzeau, Jean-Yves
author_facet Moulin, David
Salone, Véronique
Koufany, Meriem
Clément, Thomas
Behm-Ansmant, Isabelle
Branlant, Christiane
Charpentier, Bruno
Jouzeau, Jean-Yves
author_sort Moulin, David
collection PubMed
description 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.
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spelling pubmed-54583732017-06-13 MicroRNA-29b Contributes to Collagens Imbalance in Human Osteoarthritic and Dedifferentiated Articular Chondrocytes Moulin, David Salone, Véronique Koufany, Meriem Clément, Thomas Behm-Ansmant, Isabelle Branlant, Christiane Charpentier, Bruno Jouzeau, Jean-Yves Biomed Res Int Research Article 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. Hindawi 2017 2017-05-22 /pmc/articles/PMC5458373/ /pubmed/28612031 http://dx.doi.org/10.1155/2017/9792512 Text en Copyright © 2017 David Moulin et al. https://creativecommons.org/licenses/by/4.0/ 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.
spellingShingle Research Article
Moulin, David
Salone, Véronique
Koufany, Meriem
Clément, Thomas
Behm-Ansmant, Isabelle
Branlant, Christiane
Charpentier, Bruno
Jouzeau, Jean-Yves
MicroRNA-29b Contributes to Collagens Imbalance in Human Osteoarthritic and Dedifferentiated Articular Chondrocytes
title MicroRNA-29b Contributes to Collagens Imbalance in Human Osteoarthritic and Dedifferentiated Articular Chondrocytes
title_full MicroRNA-29b Contributes to Collagens Imbalance in Human Osteoarthritic and Dedifferentiated Articular Chondrocytes
title_fullStr MicroRNA-29b Contributes to Collagens Imbalance in Human Osteoarthritic and Dedifferentiated Articular Chondrocytes
title_full_unstemmed MicroRNA-29b Contributes to Collagens Imbalance in Human Osteoarthritic and Dedifferentiated Articular Chondrocytes
title_short MicroRNA-29b Contributes to Collagens Imbalance in Human Osteoarthritic and Dedifferentiated Articular Chondrocytes
title_sort microrna-29b contributes to collagens imbalance in human osteoarthritic and dedifferentiated articular chondrocytes
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5458373/
https://www.ncbi.nlm.nih.gov/pubmed/28612031
http://dx.doi.org/10.1155/2017/9792512
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