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J. Biol. Chem., Vol. 277, Issue 35, 31612-31622, August 30, 2002
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From the The differentiation of chondrocytes and of
several other cell types is associated with a switch from the
Integrins
6A
1 and
6B1 Promote Different Stages of
Chondrogenic Cell Differentiation*
,,,, and
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
6B to the 6A isoform of the laminin
6
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 6B,
adherent chondrogenic cells differentiate to stage I chondrocytes
(i.e. increased type II collagen, reduced type I collagen,
fibronectin, 51 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
6A induces an incomplete differentiation to stage I
chondrocytes, whereas no differentiation was observed in
5 and mock-transfected control cells; (iv) a prevalence
of the 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 6B to 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.
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