Chronic exposure of bone morphogenetic protein-2 favors chondrogenic expression in human articular chondrocytes amplified in monolayer cultures
Articular cartilage is a specialized connective tissue containing chondrocytes embedded in a network of extracellular macromolecules such as type II collagen and presents poor capacity to self‐repair. Autologous chondrocyte transplantation (ACT) is worldwide used for treatment of focal damage to art...
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Published in | Journal of cellular biochemistry Vol. 111; no. 6; pp. 1642 - 1651 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Hoboken
Wiley Subscription Services, Inc., A Wiley Company
15.12.2010
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Subjects | |
Online Access | Get full text |
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Summary: | Articular cartilage is a specialized connective tissue containing chondrocytes embedded in a network of extracellular macromolecules such as type II collagen and presents poor capacity to self‐repair. Autologous chondrocyte transplantation (ACT) is worldwide used for treatment of focal damage to articular cartilage. However, dedifferentiation of chondrocytes occurs during the long term culture necessary for mass cell production. The aim of this study was to investigate if addition of bone morphogenetic protein (BMP)‐2, a strong inducer of chondrogenic expression, to human chondrocytes immediately after their isolation from cartilage, could help to maintain their chondrogenic phenotype in long‐term culture conditions. Human articular chondrocytes were cultured according to the procedure used for ACT. Real‐time PCR and Western blotting were performed to evaluate the cellular phenotype. Exogenous BMP‐2 dramatically improves the chondrogenic character of knee articular chondrocytes amplified over two passages, as assessed by the BMP‐2 stimulation on type II procollagen expression and synthesis. This study reveals that BMP‐2 could potentially serve as a therapeutic agent for supporting the chondrogenic phenotype of human articular chondrocytes expanded in the conditions generally used for ACT. J. Cell. Biochem. 111: 1642–1651, 2010. © 2010 Wiley‐Liss, Inc. |
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Bibliography: | istex:5FD22F47042E5DA62E0CE2C95A38D32B8EB82F1D The authors state no conflict of interest. CNRS Société Française de Rhumatologie - No. SFR 2007 ArticleID:JCB22897 ANR TecSan - No. PROMOCART 2006 Université Lyon 1 - No. BQR 2006 ark:/67375/WNG-F2XVJL5X-J ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 |
ISSN: | 0730-2312 1097-4644 1097-4644 |
DOI: | 10.1002/jcb.22897 |