Expression of decorin and biglycan by rabbit articular chondrocytes.

Regulation of the chondrocyte phenotype by beta-catenin

“…However, we could not detect any increase of alkaline phosphatase activity in LiCl-treated micromass culture of mesenchymal cells and in articular chondrocytes treated with RA or IL1β or transfected with S37A β-catenin (data not shown), indicating that the loss of type II collagen expression is due to inhibition of chondrogenesis of mesenchymal cells and de-differentiation of articular chondrocytes. Our results are in good agreement with the observations by others, which indicate expression of hypertrophic chondrocyte markers (type X collagen and alkaline phosphatase) during micromass culture of mesenchymal cells needs much longer culture period (1-3 weeks) (Mello and Tuan, 1999;Boskey et al, 2002), and that treatment with RA (Cash et al, 1997;Hering, 1999;Weston et al, 2000), IL1β (Goldring et al, 1994;Demoor-Fossard et al, 1998) or a serial subculture (Lefebvre et al, 1990;Yoon et al, 2002) causes de-differentiation of articular chondrocytes. On the bases of the experiments by Hartmann and Tabin (Hartmann and Tabin, 2000) that suggest β-catenin misexpression promotes chondrocyte maturation and on our in vitro experiment that indicates inhibition of chondrogenesis by the accumulation of β-catenin in chondrifying mesenchymal cells, it is possible that β-catenin inhibits initial chondrogenic differentiation of mesenchymal cells and also promotes maturation of the differentiated chondrocytes that is caused by escaping from β-catenin inhibition of chondrogenesis.…”

“…The differentiated chondrocyte phenotype in normal mature cartilage is characterized by the synthesis and maintenance of cartilagespecific extracellular matrix (ECM) molecules, including type II collagen and sulfated proteoglycan. The differentiated phenotypes of chondrocytes are unstable, with rapid loss of their markers by exposure to interleukin (IL)-1β (Goldring et at al., 1994;Demoor-Fossard et al, 1998) and retinoic acid (RA) (Cash et al, 1997;Weston et al, 2000) or during in vitro culture (Lefebvre et al, 1990;Yoon et al, 2002). The dedifferentiated cells redifferentiate to chondrocytes when cultured three-dimensionally (Bonaventure et al, 1994;Yoon et al, 2002).…”

“…RA is a well-characterized soluble mediator that inhibits chondrogenesis and induces de-differentiation of chondrocytes (Cash et al, 1997;Hering, 1999;Weston et al, 2000). IL1β plays a major role in joint cartilage destruction in arthritis and induces de-differentiation of chondrocytes by inhibiting expression of cartilage-specific type II collagen and proteoglycan (Goldring et al, 1994;Demoor-Fossard et al, 1998).…”

Development and Aging of the Articular Cartilage of the Rabbit Knee Joint: Distribution of Biglycan, Decorin, and Matrilin-1

“…cDNA probes to human biglycan and decorin were a gift from Dr. L. Fisher (NIH; Bethesda, MD). These probes recognized the appropiate rabbit mRNAs on Northern blots (Demoor-Fossard et al 1998). Antisense and sense probes were generated by linearizing with Kpn I and T3 polymerase and Xba I and T7 polymerase, respectively, for biglycan and Bam HI and T7 polymerase and Kpn I and T3 polymerase, respectively, for decorin.…”

Down-regulation of Human Type II Collagen Gene Expression by Transforming Growth Factor-β1 (TGF-β1) in Articular Chondrocytes Involves SP3/SP1 Ratio

“…TGF-␤1, 1 a multifunctional regulatory cytokine, generally stimulates cell growth and production of extracellular matrix in mesenchymal cells (1)(2)(3)(4)(5)(6). It is produced by chondrocytes and abundantly stored in cartilage extracellular matrix, where it may contribute to the repair process in response to a variety of stimuli (7)(8)(9).…”