Astrocytes and endothelinergic signaling in retinal diseases

SUBURO, AM

Montreal

Simposio; Astrocytes in the retina; 2010

XIX Biennial Meeting of the International Society of Eye Research

Severe glial remodeling is one of the hallmarks of retinal diseases. Activation responses originated in Müller glial cells are the best known, since most retinal glial cells have the Müller phenotype. Retinal astrocytes constitute a smaller population. However, because of their selective association with blood vessels, astrocytes are highly involved in the course of several retinal diseases, such as retinal detachment and proliferative vitreoretinopathy, hypertensive retinopathy, diabetic retinopathy and uveitis. In normal retina, astrocytes store endothelins and express the endothelinergic receptor B. Moreover, astrocytic endothelin is involved in the regulation of the blood-retinal barrier. We evaluated the role of endothelins in the initial astrocytic response to retinal injury induced by retinal detachment or endotoxin in rodent models. To achieve this goal, we studied the activation of molecules from stress-related pathways: phosphorylation of c-Jun NH2-terminal kinase (JNK) and nuclear translocation of NFKB. We compared the activation of these pathways in astrocytes and Müller cells during the acute phase. In addition, we used tezosentan, an endothelinergic receptor blocker, to detect endothelinergic-dependent changes on the activation of stress-related molecules. Our findings suggest that astrocytic endothelinergic signaling would be involved in the initial response of the retina to retinal detachment and inflammatory conditions