Keloid fibroblasts exhibit an altered response to TGF-beta.
Treatment with transforming growth factor beta 1 (TGF-beta 1) results in stimulation of total protein synthesis in normal dermal fibroblasts but not in keloid fibroblasts, suggesting that the TGF-beta regulatory program is altered in keloid fibroblasts. However, both keloid and normal fibroblasts treated with TGF-beta 1 exhibit accelerated fibronectin biosynthesis, indicating that keloid cells can respond to TGF-beta 1. In the absence of serum, the TGF-beta 1-induced increase in fibronectin biosynthesis occurs more rapidly in keloid fibroblasts, also suggesting modification of this regulatory pathway. The TGF-beta 1-mediated increase in keloid fibronectin production is independent of the steroid regulatory pathway for fibronectin, which accelerates synthesis by means of a post-transcriptional mechanism. Thus, TGF-beta 1 stimulation of fibronectin production in keloid cells is likely to involve a transcriptional mechanism and keloid overproduction of extracellular matrix components may be due to an inherent modification of the TGF-beta regulatory program.
Babu
M
M
Department of Anatomy and Cell Biology, Tufts University School of Medicine, Boston, MA 02111.
Diegelmann
R
R
Oliver
N
N
D000293:Adolescent; D000328:Adult; D002461:Cell Line, Transformed; D005260:Female; D005347:Fibroblasts / Q000187:drug effects; D005786:Gene Expression Regulation; D006801:Humans; D007627:Keloid / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D016212:Transforming Growth Factor beta / Q000235:genetics / Q000494:pharmacology*
D016212:Transforming Growth Factor beta