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Updated: Aug 8, 2026

Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling
07:49

Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling

Published on: August 3, 2018

Gene expression in normal and doxorubicin-impaired wounds: importance of transforming growth factor-beta

G D Salomon1, A Kasid, E Bernstein

  • 1Surgery Branch, National Cancer Institute/NIH, Bethesda, MD 20892.

Surgery
|August 1, 1990
PubMed

Insights

Doxorubicin impairs wound healing by reducing transforming growth factor-beta (TGF-beta) and collagen gene expression. Topical TGF-beta application restored normal collagen levels, suggesting it can correct doxorubicin-induced healing defects.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Wound Healing Research

Background:

  • Transforming growth factor-beta (TGF-beta) is implicated in cell growth and tissue repair, but its in vivo function is unclear.
  • Doxorubicin, an antitumor drug, negatively impacts wound healing processes.

Purpose of the Study:

  • To investigate the role of TGF-beta in wound healing.
  • To determine the effect of doxorubicin on TGF-beta and collagen gene expression during wound healing.
  • To evaluate the efficacy of exogenous TGF-beta in counteracting doxorubicin's detrimental effects on wound healing.

Main Methods:

  • Analysis of messenger RNA (mRNA) expression for TGF-beta and type 1 collagen in rat wounds using complementary DNA probes.
  • Comparison of gene expression in rats treated with saline solution versus doxorubicin.
  • Administration of exogenous TGF-beta or vehicle to doxorubicin-treated rat wounds to assess its impact on collagen mRNA levels.

Main Results:

  • In saline-treated rats, TGF-beta mRNA peaked on day 7, with elevated levels on days 3 and 10; collagen mRNA was elevated on days 7 and 10.
  • Doxorubicin significantly decreased TGF-beta and collagen mRNA expression on all measured days.
  • Topical TGF-beta application in doxorubicin-treated wounds normalized or increased collagen mRNA levels.

Conclusions:

  • Doxorubicin-induced impairment of wound healing may stem from reduced TGF-beta gene expression.
  • Topical application of TGF-beta can potentially reverse the negative effects of doxorubicin on wound healing by restoring collagen synthesis.

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