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Keloid fibroblasts exhibit an altered response to TGF-beta
M Babu1, R Diegelmann, N Oliver
1Department of Anatomy and Cell Biology, Tufts University School of Medicine, Boston, MA 02111.
The Journal of Investigative Dermatology
|November 1, 1992
Summary
Transforming growth factor beta 1 (TGF-beta 1) affects protein synthesis differently in normal versus keloid fibroblasts. Keloid cells show altered TGF-beta 1 regulation, potentially explaining excessive extracellular matrix production.
Area of Science:
- Dermatology
- Cell Biology
- Biochemistry
Background:
- Keloid fibroblasts exhibit altered responses to growth factors compared to normal fibroblasts.
- Transforming growth factor beta 1 (TGF-beta 1) is a key regulator of extracellular matrix production.
Purpose of the Study:
- To investigate the differential effects of TGF-beta 1 on protein synthesis in normal and keloid fibroblasts.
- To elucidate the regulatory mechanisms underlying fibronectin biosynthesis in keloid cells.
Main Methods:
- Treatment of normal and keloid dermal fibroblasts with TGF-beta 1.
- Analysis of total protein synthesis and fibronectin biosynthesis.
- Investigation of the role of serum and steroid regulatory pathways.
Main Results:
- TGF-beta 1 stimulated total protein synthesis in normal fibroblasts but not keloid fibroblasts.
- Both cell types showed accelerated fibronectin biosynthesis upon TGF-beta 1 treatment.
- TGF-beta 1-induced fibronectin increase was faster in keloid fibroblasts, especially without serum.
- The TGF-beta 1 effect on keloid fibronectin is independent of the steroid pathway, suggesting transcriptional regulation.
Conclusions:
- Keloid fibroblasts possess an altered TGF-beta 1 regulatory program affecting protein synthesis.
- TGF-beta 1 stimulation of fibronectin production in keloid cells likely involves a transcriptional mechanism.
- Modified TGF-beta 1 signaling may contribute to the overproduction of extracellular matrix in keloids.