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Extracellular collagen regulates expression of transforming growth factor‐β1 gene
Author(s) -
Qi WenNing,
Scully Sean P.
Publication year - 2000
Publication title -
journal of orthopaedic research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.041
H-Index - 155
eISSN - 1554-527X
pISSN - 0736-0266
DOI - 10.1002/jor.1100180612
Subject(s) - transforming growth factor , extracellular , extracellular matrix , growth factor , transforming growth factor, beta 3 , transforming growth factor beta , biology , gene expression , microbiology and biotechnology , chemistry , type i collagen , tgf alpha , endocrinology , biochemistry , gene , receptor
A complex interrelationship exists between the extracellular matrix and cytokine signaling in articular chondrocytes. We sought to determine whether the extracellular matrix serves as a regulatory component of transforming growth factor‐β1 expression. Bovine articular chondrocytes were isolated and resuspended in alginate, yielding final extracellular protein concentrations of 0 to 1.5% (wt/vol) for type‐II or type‐I collagen. Cultures were maintained for 7 days in the presence or absence of transforming growth factor‐β1‐supplemented medium (10 ng/ml). The amount of transforming growth factor‐β1 mRNA was examined with quantitative competitive reverse transcription‐polymerase chain reaction analysis. The results indicate that exogenous transforming growth factor‐β1 stimulates endogenous transforming growth factor‐β1 mRNA expression approximately 8‐fold. This effect depended on the concentration of extracellular type‐II collagen. As the concentration of extracellular type‐II collagen is increased, the expression of transforming growth factor‐β1 mRNA decreases in both basal and transforming growth factor‐β1‐stimulated cultures. Exogenous extracellular type‐I collagen also served to negatively modulate transforming growth factor‐β1 gene expression but with a different concentration profile. The results demonstrate that transforming growth factor‐β1 mRNA expression was upregulated by exogenous transforming growth factor‐β1 and was downregulated by extracellular type‐I and type‐II collagens. The profoundly different effects on transforming growth factor‐β1 expression by the two collagens are consistent with those reported for mammary epithelial cells and likely serve as a negative feedback mechanism to preserve tissue homeostasis.