Type IX Collagen Gene Expression During Limb Cartilage Differentiation

Kulyk, William M.; Coelho, Caroline N.D.; Kosher, Robert A.

doi:10.1016/s0934-8832(11)80236-2

Cited by 54 publications

(50 citation statements)

References 28 publications

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“…Although fibronectin is present in cartilage matrix, it is a major component of the ECM of condensing pre-chondrogenic mesenchymal cells (Kulyk et al, 1989b). When cultures were treated with these growth factors we found that, in contrast to the effect on the steady state levels of cytoplasmic mRNA for aggrecan core protein and type I1 collagen, the effect of TGF-P on steady state levels of cytoplasmic mRNA for fibronectin is significantly greater than controls a t all time points.…”

Section: Effect Of Adding Growth Factors At Different Stages Of Cartimentioning

confidence: 55%

Transforming growth factor‐β and bone morphogenetic protein‐2 act by distinct mechanisms to promote chick limb cartilage differentiation in vitro

Roark

Greer

1994

Developmental Dynamics

129

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A number of studies suggest that several members of the transforming growth factor‐β (TGF‐β) family of peptide growth factors may be involved in the regulation of cartilage differentiation. It has been previously reported that TGF‐β1 and TGF‐β2 promote the chondrogenic differentiation of chick limb mesenchymal cells in high density micromass cultures (Kulyk et al. [1989a] Dev. Biol. 135:424–430). In this study we report that chick limb mesenchymal cells express mRNA for chicken TGF‐β1, TGF‐β2, and TGF‐β3 during cartilage differentiation in vitro. In addition, the time course of their expression during cartilage differentiation is consistent with their playing a role in the initiation of this differentiation process. We also report that two members of the TGF‐β family, TGF‐β3 and bone morphogenetic protein‐2 (BMP‐2), are capable of promoting the accumulation of cartilage extracellular matrix molecules by differentiating chick limb mesenchymal cells in micromass culture. Significant differences, however, were noted between the specific effects on matrix production elicited by these two growth factors which suggest that they may be acting by distinct mechanisms to regulate cartilage matrix production. TGF‐β appears to be most effective on cells which have not yet undergone cell condensation, a critical event in early cartilage differentiation, wherease BMP‐2 is most effective after cells have condensed or differentiated. These observations suggest that TGF‐β3 and BMP‐2 may be acting in a sequential manner to regulate chick limb mesenchymal cells through the different stages of cartilage differentiation. © 1994 Wiley‐Liss, Inc.

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Section: Effect Of Adding Growth Factors At Different Stages Of Cartimentioning

confidence: 55%

Transforming growth factor‐β and bone morphogenetic protein‐2 act by distinct mechanisms to promote chick limb cartilage differentiation in vitro

Roark

Greer

1994

Developmental Dynamics

129

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“…The mechanism by which these hyaluronan-based implants enhance the natural response is unclear. On the basis of the many biological roles attributable to the components of the implants (17,(30)(31)(32)37,48,49,54,55), there are several possible explanations for the observations presented here. Pretreatment of materials with fibronectin has been shown to have a positive effect on cell attachment and retention (14).…”

Section: A Solchaga Et a Lmentioning

confidence: 89%

Hyaluronan‐based polymers in the treatment of osteochondral defects

Solchaga

Yoo

Lundberg

et al. 2000

Journal Orthopaedic Research

212

131

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Summary: Articular cartilage in adults has limited ability for self-repair. Some methods devised to augment the natural healing response stimulate some regeneration, but the repair is often incomplete and lacks durability. Hyaluronan-based polymers were tested for their ability to enhance the natural healing response. It is hypothesized that hyaluronan-based polymers recreate an embryonic-like milieu where host progenitor cells can rcgcncrate the damaged articular surface and underlying bone. Oskochondral dcfccts were made on the femoral condyles of 4-month-old rabbits and were left empty or filled with hyaluronan-based polymers. The polymers tested were ACP sponge. made of crosslinked hyaluronan, and HYAFF-11 sponge, made of benxylated hyaluronan. The rabbits were killed 4 and 12 weeks after surgery, and the condyles were processed for histology. All 12-week defects were scored with a 29-point scale, and the scores were compared with a Kruskall-Wallis analysis of variance on ranks. Untreated defects filled with bone tissue up to or beyond the tidemark, and the noncalcified surface layer varied from fibrous to hyaline-like tissue. Four weeks aftcr surgery, defects treated with ACP exhibited bone filling to the level of the tidemark and the surface layer was composed of hyaline-like cartilage well integrated with the adjacent cartilage. At 12 weeks, the specimens had bone beyond the tidemark that was covered with a thin layer of hyaline cartilage. Four weeks after surgery, defects treated with HYAFF-11 contained a rim of chondrogcnic cells at the interface of the implant and the host tissue. In general, the 12-week dcfccts exhibited good bone fill and the surface was mainly hyaline cartilage. Treated defects received significantly higher scores than untreated defects (p < 0.05), and ACP-trcatcd defects scored significantly higher than HYAFF-11-treated defects (p < 0.05). The introduction of these hyaluronan-based polymers into delects provides an appropriate scaffolding and favorable microenvironnient for the reparative process. Further work is required to lully assess thc long-term outcome of defects treated with these polymers.The successful regeneration of any tissue requires not oiily reparative cells with the potential to differentiate into the phenotypes required to restore the damaged site but also a microenvironment that supports the proliferation and differentiation of those cells (12). It is our hypothesis that these reparative cells recapitulate, a t least in part. the sequence of events that leads to the formation of differentiated tissues during embryonic development; therefore. materials that mimic an embryonic environment may be superior scaffolds for tissue-engineered repair of damaged tissues.Articular cartilage has no vascular supply or easy access to large quantities of progenitor cells: thus, cartilage repair is often unsuccessful. Some studies indicate that full-thickness lesions in young animals are

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“…One of the key features of chondrogenesis is a temporal change in the composition of the deposited ECM . During condensation, matrix proteins such as fibronectin, collagen I and the proteoglycan versican are prevalent (Dessau et al, 1980;Kamiya et al, 2006;Kimata et al, 1986;Kulyk et al, 1991). In contrast, matrix deposited by differentiated chondrocytes is rich in collagens II and IX and the proteoglycan aggrecan (Choocheep et al, 2010;Knudson and Knudson, 2001;Knudson and Toole, 1985;Kravis and Upholt, 1985;Kulyk et al, 1991); this matrix might provide the optimal stiffness, which is known to be important for chondrocyte differentiation (Allen et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

“…Upregulation of the cell-cell adhesion proteins N-cadherin and neural cell adhesion molecule (N-CAM) is a hallmark of condensing cells (Bobick et al, 2009;Singh and Schwarzbauer, 2012) and condensation is reduced with loss of N-cadherin function (Bobick et al, 2009;DeLise and Tuan, 2002a;DeLise and Tuan, 2002b). Among the matrix proteins, fibronectin is abundant in mesenchyme and is upregulated during condensation in vivo and in vitro (Dessau et al, 1980;Kulyk et al, 1989). Interactions involving the N-terminal domain of fibronectin and heparinase-sensitive molecules on mesenchymal cell surfaces have been implicated in condensation (Frenz et al, 1989).…”

Section: Introductionmentioning

confidence: 99%

Fibronectin matrix assembly is essential for cell condensation during chondrogenesis

Singh

Schwarzbauer

2014

Journal of Cell Science

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Mesenchymal cell condensation is the initiating event in endochondral bone formation. Cell condensation is followed by differentiation into chondrocytes, which is accompanied by induction of chondrogenic gene expression. Gene mutations involved in chondrogenesis cause chondrodysplasias and other skeletal defects. Using mesenchymal stem cells (MSCs) in an in vitro chondrogenesis assay, we found that knockdown of the diastrophic dysplasia (DTD) sulfate transporter (DTDST, also known as SLC26A2), which is required for normal cartilage development, blocked cell condensation and caused a significant reduction in fibronectin matrix. Knockdown of fibronectin with small interfering RNAs (siRNAs) also blocked condensation. Fibrillar fibronectin matrix was detected prior to cell condensation, and its levels increased during and after condensation. Inhibition of fibronectin matrix assembly by use of the functional upstream domain (FUD) of adhesin F1 from Streptococcus pyogenes prevented cell condensation by MSCs and also by the chondrogenic cell line ATDC5. Our data show that cell condensation and induction of chondrogenesis depend on fibronectin matrix assembly and DTDST, and indicate that this transporter is required earlier in chondrogenesis than previously appreciated. They also raise the possibility that certain of the skeletal defects in DTD patients might derive from the link between DTDST, fibronectin matrix and condensation.

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Type IX Collagen Gene Expression During Limb Cartilage Differentiation

Cited by 54 publications

References 28 publications

Transforming growth factor‐β and bone morphogenetic protein‐2 act by distinct mechanisms to promote chick limb cartilage differentiation in vitro

Transforming growth factor‐β and bone morphogenetic protein‐2 act by distinct mechanisms to promote chick limb cartilage differentiation in vitro

Hyaluronan‐based polymers in the treatment of osteochondral defects

Fibronectin matrix assembly is essential for cell condensation during chondrogenesis

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