Expression of β-catenin and cyclin D1 in epidermal stem cells of diabetic rats

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Qing-Ling Zhong1, Fan-Rong Liu, De-Wu Liu

  • 1Burns Institute, Nanchang University Medical College, Nanchang, P.R. China.

Molecular Medicine Reports
|April 7, 2011
PubMed

Insights

Diabetic wound healing is impaired due to reduced epidermal stem cell (ESC) activity. This study found lower expression of beta-catenin and cyclin D1 in diabetic rat ESCs, contributing to delayed healing in diabetes mellitus.

Area of Science:

  • Biomedical research
  • Molecular biology
  • Wound healing research

Background:

  • Diabetic wound healing presents significant clinical challenges.
  • The underlying molecular mechanisms of impaired wound healing in diabetes mellitus (DM) remain unclear.

Purpose of the Study:

  • To investigate the expression of beta-catenin and cyclin D1 in epidermal stem cells (ESCs) of diabetic rats.
  • To explore the role of reduced beta-catenin and cyclin D1 in the poor wound healing observed in DM.

Main Methods:

  • Comparative analysis of ESCs from diabetic and control rats.
  • Assessment of ESC quantity, clone formation efficiency, and mRNA/protein expression levels of beta-catenin and cyclin D1.

Main Results:

  • Diabetic rat ESCs were reduced in number and exhibited lower clone formation efficiency compared to controls.
  • Significant decrease in both mRNA and protein expression of beta-catenin and cyclin D1 was observed in diabetic rat ESCs.

Conclusions:

  • Reduced expression of beta-catenin and cyclin D1 may decrease the activity of ESCs in diabetic rats.
  • This downregulation of beta-catenin and cyclin D1 is a potential key mechanism contributing to delayed wound healing in diabetes mellitus.

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