Immunophenotypic analysis of human articular chondrocytes: Changes in surface markers associated with cell expansion in monolayer culture
Article first published online: 18 AUG 2004
Copyright © 2004 Wiley-Liss, Inc.
Journal of Cellular Physiology
Volume 202, Issue 3, pages 731–742, March 2005
How to Cite
Diaz-Romero, J., Gaillard, J. P., Grogan, S. P., Nesic, D., Trub, T. and Mainil-Varlet, P. (2005), Immunophenotypic analysis of human articular chondrocytes: Changes in surface markers associated with cell expansion in monolayer culture. J. Cell. Physiol., 202: 731–742. doi: 10.1002/jcp.20164
- Issue published online: 27 DEC 2004
- Article first published online: 18 AUG 2004
- Manuscript Accepted: 1 JUN 2004
- Manuscript Received: 21 NOV 2003
- Swiss Commission for Technology and Innovation. Grant Number: KTI 4716.1
- OncoSwiss. Grant Number: OCS 1190-9-2001
Cartilage tissue engineering relies on in vitro expansion of primary chondrocytes. Monolayer is the chosen culture model for chondrocyte expansion because in this system the proliferative capacity of chondrocytes is substantially higher compared to non-adherent systems. However, human articular chondrocytes (HACs) cultured as monolayers undergo changes in phenotype and gene expression known as “dedifferentiation.” To gain a better understanding of the cellular mechanisms involved in the dedifferentiation process, our research focused on the characterization of the surface molecule phenotype of HACs in monolayer culture. Adult HACs were isolated by enzymatic digestion of cartilage samples obtained post-mortem. HACs cultured in monolayer for different time periods were analyzed by flow cytometry for the expression of cell surface markers with a panel of 52 antibodies. Our results show that HACs express surface molecules belonging to different categories: integrins and other adhesion molecules (CD49a, CD49b, CD49c, CD49e, CD49f, CD51/61, CD54, CD106, CD166, CD58, CD44), tetraspanins (CD9, CD63, CD81, CD82, CD151), receptors (CD105, CD119, CD130, CD140a, CD221, CD95, CD120a, CD71, CD14), ectoenzymes (CD10, CD26), and other surface molecules (CD90, CD99). Moreover, differential expression of certain markers in monolayer culture was identified. Up-regulation of markers on HACs regarded as distinctive for mesenchymal stem cells (CD10, CD90, CD105, CD166) during monolayer culture suggested that dedifferentiation leads to reversion to a primitive phenotype. This study contributes to the definition of HAC phenotype, and provides new potential markers to characterize chondrocyte differentiation stage in the context of tissue engineering applications. © 2004 Wiley-Liss, Inc.