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Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
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Downregulation of apoptosis-related genes in keloid tissues

D N Sayah1, C Soo, W W Shaw

  • 1Institute of Reconstructive Plastic Surgery, New York University, New York, New York 10016, USA.

The Journal of Surgical Research
|December 22, 1999
PubMed
Abstract

Insights

Keloid tissue shows reduced expression of apoptosis-related genes, leading to fewer dying cells. This suggests keloid fibroblasts resist programmed cell death, causing abnormal scar growth.

Area of Science:

  • Molecular Biology
  • Dermatology
  • Cell Biology

Background:

  • Apoptosis, or programmed cell death, is crucial for maintaining tissue homeostasis by balancing cell proliferation and demise.
  • Keloids are abnormal scars characterized by excessive connective tissue deposition, suggesting a potential disruption in normal cell death processes.

Purpose of the Study:

  • To investigate the role of apoptosis in keloid formation by comparing apoptosis-related gene expression in keloid and normal scar tissues.
  • To evaluate the rate of apoptotic cell death in keloid fibroblasts compared to normal scar fibroblasts.

Main Methods:

  • Compared the expression of 64 apoptosis-related genes in keloid and normal scar tissues using human cDNA arrayed hybridization.
  • Quantified the percentage of apoptotic cells in keloid (center and periphery) and normal scar tissues using TUNEL assays.

Main Results:

  • Eight apoptosis-related genes were significantly underexpressed in keloid tissue compared to normal scar tissue.
  • Specific underexpressed genes include DAD-1, NDKB, GSTs, GPx, TRADD, NIP3, and HDLC1.
  • TUNEL assays indicated lower apoptosis indices in keloid tissue (0.63-0.83) compared to normal scars.

Conclusions:

  • Keloid tissue exhibits underexpression of apoptosis-related genes and reduced apoptotic activity in fibroblasts.
  • This suggests keloid fibroblasts may evade programmed cell death, leading to excessive connective tissue production and hypertrophic scarring.
  • Targeting apoptosis pathways presents a potential therapeutic strategy for treating keloids.

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