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Originally published In Press as doi:10.1074/jbc.M203471200 on June 19, 2002

J. Biol. Chem., Vol. 277, Issue 35, 31612-31622, August 30, 2002
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Integrins alpha 6Abeta 1 and alpha 6Bbeta 1 Promote Different Stages of Chondrogenic Cell Differentiation*

Daniela SegatDagger , Riccardo ComaiDagger , Eddi Di Marco§, Antonella StrangioDagger , Ranieri Cancedda§, Adriano T. FranziDagger , and Carlo TacchettiDagger ||

From the Dagger  Dipartimento di Medicina Sperimentale, Sezione di Anatomia Umana, and  Dipartimento Oncologia, Biologia e Genetica, Universita' di Genova and the § Istituto Nazionale per la Ricerca sul Cancro, Centro di Biotecnologie Avanzate, Laboratorio Differenziamento Cellulare, 16100 Genova, Italy

The differentiation of chondrocytes and of several other cell types is associated with a switch from the alpha 6B to the alpha 6A isoform of the laminin alpha 6beta 1 integrin receptor. To define whether this event plays a functional role in cell differentiation, we used an in vitro model system that allows chick chondrogenic cells to remain undifferentiated when cultured in monolayer and to differentiate into chondrocytes when grown in suspension culture. We report that: (i) upon over-expression of the human alpha 6B, adherent chondrogenic cells differentiate to stage I chondrocytes (i.e. increased type II collagen, reduced type I collagen, fibronectin, alpha 5beta 1 and growth rate, loss of fibroblast morphology); (ii) the expression of type II collagen requires the activation of p38 MAP kinase; (iii) the over-expression of alpha 6A induces an incomplete differentiation to stage I chondrocytes, whereas no differentiation was observed in alpha 5 and mock-transfected control cells; (iv) a prevalence of the alpha 6A subunit is necessary to stabilize the differentiated phenotype when cells are transferred to suspension culture. Altogether, these results indicate a functional role for the alpha 6B to alpha 6A switch in chondrocyte differentiation; the former promotes chondrocyte differentiation, and the latter is necessary in stabilizing the differentiated phenotype.


* This work was supported by grants from MURST (PRIN projects) and CNR (Target project Biotechnology) (to C. T.). The monoclonal antibodies V2E9 and B3D6 were obtained, respectively, from the Developmental Studies Hybridoma Bank, maintained at the Department of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, and the Department of Biological Sciences, University of Iowa, Iowa City, under contract NO1-HD-2-3144 from the NICHD, National Institutes of Health.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

|| To whom correspondence should be addressed: Dipartimento di Medicina Sperimentale, Sezione di Anatomia Umana, Università di Genova, Via de Toni, 14 16100 Genova, Italy. Tel.: 39-0103537864; Fax: 39-0103537885; E-mail: carlo.tacchetti@unige.it.


Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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