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- W4313404894 abstract "Abstract Diabetic retinopathy (DR), an incurable eye disease, is a common complication of diabetes mellitus and the leading cause of blindness amongst working age adults. Prolonged high glucose levels damage retinal blood vessels leading to hemorrhages, ischemia and ultimately vision loss. Microglia, the resident macrophages of the central nervous system, are rapidly activated and respond to transient hyperglycemia, and reset the homeostatic threshold of the retina. As hyperglycemia persists, capillary damage occurs resulting in serum proteins and DAMPs from the periphery leaking into the retina perpetuating microgliosis, pro-inflammatory cytokine production and vascular damage that correlates with neuronal loss. Therefore, we transiently depleted microglia to determine the mechanism by which resident retinal macrophages regulate neuronal and vascular damage at early stages of diabetes. We hypothesize that transient depletion of CX3CR1CreER:R26iDTR microglia during the course of disease when microglia receive the early-stage environmental cues of retinal inflammation due to hyperglycemia will induce neuroprotective cues. Utilizing a genetic model to express diphtheria toxin receptor under the tamoxifen inducible CX3CR1-promoter, microglia become susceptible to the effects of diphtheria toxin. Our findings revealed that transient depletion of microglia induced neuroprotective cues to upregulate TUJ1+ neurons and ameliorate vascular damage in the diabetic retina. In conclusion these studies suggest that early transient microglia depletion is neuroprotective by inducing the proliferation of a homeostatic microglia cell population that induce axonal regeneration of TUJ1+ neurons and vascular repair. Supported by grants from NIH (R01EY029913) and NIH RISE Grant (GM061655)." @default.
- W4313404894 created "2023-01-06" @default.
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- W4313404894 date "2022-05-01" @default.
- W4313404894 modified "2023-09-27" @default.
- W4313404894 title "Microglia depletion elicits neuroprotective effects to alleviate vascular damage and neuronal cell loss in the diabetic retina" @default.
- W4313404894 doi "https://doi.org/10.4049/jimmunol.208.supp.54.14" @default.
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