Diabetes: Hyperglycemia Suppresses TGF, Contributing to Delayed Wound, Corneal Healing

Fu-Shin X. Yu, Ph.D. Professor and Director of Research Kresge Eye Institute/Department of Ophthalmology Wayne State University School of Medicine Detroit, MI 48201 MedicalResearch.com Interview with:
Fu-Shin X. Yu, Ph.D.
Professor and Director of Research
Kresge Eye Institute/Department of Ophthalmology
Wayne State University School of Medicine
Detroit, MI 48201

MedicalResearch.com: What are the main results of your study?

Dr. Fu-Shin X. Yu: Using genome-wide cDNA array, we identified a large group of gene differentially expressed in healing corneal cells of diabetes mellitus, when compared to normoglycemia, corneas.

Gene ontology analysis suggests transforming growth factor (TGFβ) signaling as a major signaling pathway affected by hyperglycemia in diabetes mellitus corneal epithelial cells.

Surprisingly, we found that wound-induced upregulation of TGFβ3, but not TGFβ1, is dampened by hyperglycemia and that by adding TGFβ3 to the wound, epithelial wound closure was accelerated.

This discovery may provide new treatment options for diabetic wound healing in tissues such as the cornea and the skin.

Citation:

Genome-wide transcriptional analysis of differentially expressed genes in diabetic, healing corneal epithelial cells: hyperglycemia-suppressed TGFβ3 expression contributes to the delay of epithelial wound healing in diabetic corneas

Ilham Bettahi, Haijing Sun, Nan Gao, Feng Wang, Xiaofan Mi, Weiping Chen, Zuguo Liu, and Fu-Shin Yu

Diabetes published ahead of print December 4, 2013, doi:10.2337/db13-1260