Posted on April 18, 2016
New research from a team at Wayne State University reports a major advance in the understanding of the mechanisms underlying diabetic peripheral neuropathy (DPN) and wound healing in diabetic ulcers of the cornea and skin. The insight also provides guidance into a new therapeutic approach that may partially reverse the adverse effects of diabetes on sensory nerve regeneration. The conclusions are published in Journal of Clinical Investigation. The research is based on experiments with mouse corneas, which the team characterizes as the most densely innervated mammalian tissue and appropriate for the study of DPN mechanisms. The study found that the regenerative capacity of corneal nerves following wounding is impaired in the corneas of diabetic mice compared to normal mouse corneas. This was further associated with a dearth of infiltrating dendritic cells in the wounded corneas of diabetic mice.
These dendritic cells express ciliary neurotrophic factor (CNTF) in normal and healing corneas that helps to mediate sensory nerve innervation and regeneration. The researchers then found that the application of exogenous CNTF or its soluble receptor CNTFR-alpha can partially reverse the adverse effects of diabetes on sensory nerve regeneration. Fu-shin Yu, PhD, professor of ophthalmology and director of research at the Kresge Eye Institute of Wayne State University, commented, "These novel findings have potential to develop new dendritic cell-based cell therapy to treat diabetic peripheral neuropathy and ulcerations in the cornea and skin."
Read more about diabetic peripheral neuropathy here.
Read a news story about the new discoveries here.
The journal article may be read here.