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Reduced expression of mRNA for transforming growth factor β(TGFβ) and TGFβ receptors I and II and decreased TGFβ binding to the receptors in in vitro-aged fibroblasts

Previous studies have demonstrated that the expression of type I collagen, the most abundant protein in the dermis, is reduced in in vitro-aging fibroblast cultures, but the mechanism controlling the reduction of type I collagen expression is not understood. Recent studies, however, have demonstrate...

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Bibliographic Details
Published in:Archives of Dermatological Research 1998-03, Vol.290 (3), p.158-162
Main Authors: MORI, Y, HATAMOCHI, A, ARAKAWA, M, UEKI, H
Format: Article
Language:English
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Summary:Previous studies have demonstrated that the expression of type I collagen, the most abundant protein in the dermis, is reduced in in vitro-aging fibroblast cultures, but the mechanism controlling the reduction of type I collagen expression is not understood. Recent studies, however, have demonstrated that transforming growth factor beta (TGF beta) plays an important role in the regulation of type I collagen expression. The purpose of this study was to investigate the role of TGF beta in downregulation of type I collagen expression in in vitro-aged fibroblasts. We compared the expression of mRNA for alpha 1 (I) collagen, TGF beta, TGF beta type I receptor and TGF beta type II receptor in early and late-passage fibroblasts by Northern blot hybridizations. The mRNA levels of alpha 1(I) collagen, TGF beta, and TGF beta receptors I and II in late-passage fibroblasts were reduced to 62%, 62%, 59% and 59%, respectively, of those in early-passage fibroblasts. We also compared TGF beta receptor binding in early- and late-passage fibroblasts using receptor binding assays. The affinity of 125I-TGF beta in late-passage fibroblasts was lower than that in early-passage fibroblasts. These results suggest that the reduction of type I collagen expression in in vitro-aged fibroblasts is regulated by reduced expression of TGF beta and TGF beta receptors I and II and by decreased TGF beta receptor binding ability of the fibroblasts.
ISSN:0340-3696
1432-069X
DOI:10.1007/s004030050282