Differential profiles of pannexin-1 in diabetes and wound healing during aging
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Abstract
Diabetes mellitus is a very common disease with a global prevalence of 470 million in 2017. Diabetics have a higher risk of developing a number of complications in the cornea including dysfunctional wound healing, many of which currently have risky or limited available treatments. Aging also commonly presents with various corneal abnormalities and an altered wound healing response. The membrane pore protein pannexin-1 has been shown to release ATP into extracellular space in response to physiological stimuli which can activate local purinergic receptors such as P2X7-R. In an injured cornea, pannexin-1 and P2X7-R normally localize to the wound edge, which work synergistically with each other to induce a wound healing response. This thesis examines how the expression and post-translational modifications of pannexin-1 are altered in diabetes and aging following a wound. It was determined that pannexin-1 has more extensive glycosylation in human diabetic corneal epithelial cells compared to controls. Compared to the corneas of young mice, there was a small, non-significant increase in total pannexin-1 expression in the corneas of old mice, and pannexin-1 expression was slightly reduced following a wound in both age cohorts. These results indicate changes in pannexin-1 in diabetes and potentially aging, and warrants further studies on how such alterations may contribute to the pathophysiology of these conditions in order to develop therapeutics to improve corneal wound healing.
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Attribution 4.0 International