TRPV2 and Diabetic Retinopathy: Oral presentation

Michael O'Hare, Peter Barabas, Gema Esquiva Sobrino, Mary McGahon, Jennifer Henry, Richard Knell, David Grieve, Timothy Curtis

Research output: Contribution to conferenceOther


TRPV2 is a stretch-activated transient receptor potential channel present in neurons as well as cells of the vasculature. In the retina, we have reported that TRPV2 contributes to the myogenic constriction of retinal arterial vessels, a mechanism that protects the downstream capillary beds from overt changes in pressure and flow. Diminished myogenic signalling is an early hallmark of diabetic retinopathy and our previous work has shown reduced TRPV2 channel expression and activity in rodent models of diabetes. Here we report that TRPV2 heterozygous (+/-) rats exhibit reduced TRPV2 expression and develop retinal pathology reminiscent of diabetic retinopathy. TRPV2+/- rats were assessed for retinal pathology at postnatal days (P) 20, 90 and 360. Immunohistochemical analysis of flat-mounted retinas and retinal cryosections was performed to study the vascular, neuronal and glial components. Vasopermeability was assessed using the Evan‘s blue dye method and systemic blood pressure measured using tail cuff plethysmography. Retinal neurophysiology was examined by electroretinography (ERG). Blood glucose, haemoglobin A1c and systemic blood pressure were within normal parameters in TRPV2+/- rats. At P90 and P360, TRPV2+/- animals exhibited a significant increase in vasopermeability (P< 0.05) and acellular capillary formation (collagen IV positive/Isolectin B4 negative vessels; P< 0.05). A decrease in the mean number of retinal ganglion cells (p< 0.001) and an increase in the proportion of activated Müller glia (GFAP-positive; p< 0.0001) was also observed. In addition, microglial cell numbers were increased in P90 and P360 TRPV2+/- retinas (P< 0.05 & P< 0.01 respectively). TRPV2+/- animals also had a reduction in the amplitude of both the ERG A & B-waves at P360 (P< 0.01). TRPV2 heterozygous rats exhibit microvascular pathology without changes in blood sugar levels or blood pressure, suggesting that even partial loss of TRPV2 channels is sufficiently detrimental to cause retinal pathology. Reduced TRPV2 function may be a contributing factor to the pathogenesis of diabetic retinopathy.
Original languageEnglish
Number of pages1
Publication statusAccepted - 2018
EventXXIII Biennial Meeting of the International Society for Eye Research - Belfast, United Kingdom
Duration: 09 Sep 201813 Sep 2018


ConferenceXXIII Biennial Meeting of the International Society for Eye Research
Country/TerritoryUnited Kingdom


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