...endothelial progenitor cells (EPCs) are decreased in the circulation and at wound sites in diabetics.

Derived from the bone marrow, EPCs, which are essential for the formation of blood vessels and wound healing, would normally travel to sites of injury.

Omaida Velazquez and colleagues from University of Pennsylvania Medical Center, in their examination of diabetic mice discovered why the numbers of these important EPCs are decreased in the circulation and at wound sites in diabetes.

According to the study's authors, increased oxygen levels (hyperoxia) enhance the mobilization of EPCs from the bone marrow to the peripheral blood circulation. Also, hyperoxia increases the activation of the bone marrow enzyme eNOS (which stimulates nitric oxide production) - helping to produce greater numbers of EPCs.

But, in order to bring the EPCs from the blood circulation to the wound site, a local injection of the chemokine stromal cell-derived factor 1 alpha (SDF-1alpha) was required.

Pardon the heavy scientific jargon...but these findings will later lead to therapies for enhanced wound healing in diabetics.
In conclusion (according to the study's authors): impaired eNOS activation and decreased SDF-1alpha expression in diabetes are responsible for the defect in diabetic wound healing.

And I thought it was just because of the excessive sugar that's why wounds in diabetics heal slowly!

The study's findings have been reported in the May 1 issue of the Journal of Clinical Investigation.

Read the full report.

[Photo Credit: Metro Health]