Synthesis of type V collagen by fibroblasts derived from normal, inflamed and hyperplastic human connective tissues.
Increased type V collagen content is a feature of many inflammatory and fibroproliferative diseases. In order to understand the mechanism responsible for this increase we have studied type V collagen synthesis by fibroblasts obtained from normal, inflamed and phenytoin-hyperplastic human gingivae. Cultures were immunostained with antibodies to type V and I collagens to determine the proportion of cells producing type V collagen. In addition, cells were metabolically labeled with radioactive amino acids, and type V procollagen and collagen were fractionated and quantitated. Results showed that all the cells were stained by both anti-type V and type I antibodies. Anti-type V staining was observed outside the cells whereas anti-type I staining was localized intracellularly. The proportion of radioactive type V collagen in the individual cell strains ranged from 0-5.2% of the total collagens; however, differences among the three cell types were not statistically significant. No differences were observed in the procollagen [V] levels, which accounted for 6.5-15.1% of the total procollagens. We conclude that changes in fibroblast population may not be a significant factor contributing to increased type V collagen in inflammation and hyperplasia, and that the increase may be due to other factors such as modulation of synthesis activities by environmental ligands and resistance of type V collagen to degradation.
D002460:Cell Line; D003094:Collagen / Q000096:biosynthesis*; D003238:Connective Tissue / Q000378:metabolism*; D005347:Fibroblasts / Q000378:metabolism*; D005881:Gingiva / Q000378:metabolism*; D005885:Gingival Hyperplasia; D005891:Gingivitis / Q000378:metabolism; D006801:Humans; D011347:Procollagen / Q000096:biosynthesis
D011347:Procollagen; D003094:Collagen