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Chondrocytes isolated from tibial dyschondroplasia lesions and articular cartilage revert to a growth plate-like phenotype when cultured in vitro.
- Source :
-
Journal of cellular physiology [J Cell Physiol] 2005 Jan; Vol. 202 (1), pp. 167-77. - Publication Year :
- 2005
-
Abstract
- We report here a comparative study of the development and behavior of chondrocytes isolated from normal growth plate tissue, tibial dyschondroplasic lesions, and from articular cartilage. The objective of these studies was to determine whether the properties exhibited by chondrocytes in dysplasic lesions or in articular cartilage were due to their cellular phenotype, their environment, or both. We had previously analyzed the electrolytes and amino acid levels in the extracellular fluid of avian growth plate chondrocytes. Using these data, we constructed a culture medium (DATP5) in which growth plate cells essentially recapitulate their normal behavior in vivo. Here, we used DATP5 to examine the behavior of chondrocytes isolated from lesions of tibial dyschondroplasia (TD). We found that once isolated from lesion and grown in this supportive medium, dysplasic chondrocytes behaved essentially like normal growth plate cells. These findings suggest that the cause of TD is local factors operating in vivo to prevent these cells from developing normally. With respect to articular chondrocytes, our data indicate that they more closely retain normal protein and proteoglycan synthesis when grown in serum-free media. These cells readily induced mineral formation in vitro, both in the presence and absence of serum. However, in serum-containing media, mineralization was significantly enhanced when the cells were exposed to retinoic acid (RA) or osteogenic protein-1 (OP-1). Our studies support previous work indicating the presence of autocrine factors produced by articular chondrocytes in vivo that prevent mineralization and preserve matrix integrity. The lack of inhibitory factors and the presence of supporting factors are likely reasons for the induction of mineralization by articular chondrocytes in vitro.<br /> (2005 Wiley-Liss, Inc.)
- Subjects :
- Animals
Autocrine Communication physiology
Bone Morphogenetic Protein 7
Bone Morphogenetic Proteins metabolism
Bone Morphogenetic Proteins pharmacology
Calcification, Physiologic drug effects
Calcinosis genetics
Calcinosis metabolism
Calcinosis physiopathology
Cartilage, Articular cytology
Cartilage, Articular drug effects
Cartilage, Articular metabolism
Cell Differentiation drug effects
Cell Differentiation physiology
Cells, Cultured
Chickens
Chondrocytes cytology
Chondrocytes drug effects
Chondrogenesis drug effects
Culture Media chemistry
Culture Media pharmacology
Culture Media, Serum-Free pharmacology
Growth Plate cytology
Growth Plate drug effects
Growth Plate metabolism
Osteochondrodysplasias genetics
Osteochondrodysplasias physiopathology
Proteoglycans biosynthesis
Tibia growth & development
Tibia pathology
Tibia physiopathology
Transforming Growth Factor beta metabolism
Transforming Growth Factor beta pharmacology
Tretinoin pharmacology
Calcification, Physiologic genetics
Cartilage, Articular growth & development
Chondrocytes metabolism
Chondrogenesis physiology
Growth Plate growth & development
Osteochondrodysplasias metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 0021-9541
- Volume :
- 202
- Issue :
- 1
- Database :
- MEDLINE
- Journal :
- Journal of cellular physiology
- Publication Type :
- Academic Journal
- Accession number :
- 15389532
- Full Text :
- https://doi.org/10.1002/jcp.20105