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Yangyang Zhang, Qingjun Zhou, Lixin Xie; Role of impaired platelet function and PDGF expression in diabetic corneal epithelial regeneration. Invest. Ophthalmol. Vis. Sci. 2018;59(9):4364.
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Impaired platelet function is associated with several diabetic complications. PDGF is mainly released by platelets upon activation. We investigated the roles and mechanisms of impaired platelet function and PDGF expression in corneal epithelial regeneration of diabetic mice.
Type 1 diabetic mice were inducted by STZ and human blood came from patients. Platelet number in blood were counted and the exudation after corneal epithelial wound were observed by confocal microscopy. To deplete platelets, mice were injected intraperitoneally with anti-mouse GPIbα 24 hours before wounding. The expression of PDGF-BB in Platelet-rich Plasma（PRP）lysate were detected by immunoprecipitation and western-blot and ELISA. Exogenous PDGF-BB was topically applied to evaluate the effect on cornea epithelial regeneration. Phosphorylation ERK and AKT activation was analyzed by immunoprecipitation and western-blot.
Platelet number in blood and PDGF-BB expression in PRP lysate were decreased in diabetic than normal mice/patients. In diabetic mice, the number of platelets exudation from the limbal vessels after corneal epithelial wound was less than normal mice. Platelets depletion mice has the lower expression of PDGF-BB compared to the normal mice. PDGF-BB expression in diabetic corneal epithelium was decreased in unwound/wounded diabetic mice, as well as in platelet-depleted mice. Exogenous PDGF-BB promoted corneal epithelial wound healing in diabetic mice and normal platelet-depleted mice by activated ERK and AKT. Moreover, PRP lysate promoted the corneal wound healing in diabetic mice.
Impaired platelet function induces the decline of PDGF-BB expression and contributes to the delayed corneal epithelial regeneration in diabetic mice.
This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.
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