IGF-I-induced chronic gliosis and retinal stress lead to neurodegeneration in an animal model of retinopathy

ABSTRACT: IGF-I exert multiple effects in different retinal cell populations in both physiological and pathological conditions. Transgenic mice overexpressing IGF-I in the retina showed impaired electroretinographic responses at 6-7 months of age that worsen with age. This retinal neuronal dysfunction was correlated with the loss of rod photoreceptors, bipolar, ganglion and amacrines cells. Neuronal alterations were preceded by the overexpression of retinal stress markers, acute phase proteins and gliosis-related genes. IGF-I overexpression leads to chronic gliosis and microgliosis in TgIGF-I retinas, with mild oxidative stress, impaired recycling of glutamate and defective potassium buffering. These impaired supportive functions can contribute to neurodegeneration in TgIGF-I retinas, together with

ORGANISM(S): Mus musculus

SUBMITTER: albert ribera 

PROVIDER: E-MEXP-3786 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress