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Retinal Astrocytes Mediate Neuroprotective Effects Through p38 MAPK Dependent Activation

Astrocytes play a fundamental role in maintaining a delicate neuronal homeostasis. In response to injury and stress, astrocytes undergo a switch; becoming hypertrophic and migratory, secreting cytokines, coordinating tissue remodeling, and increasing production of antioxidants. However, the cellular signals regulating this switch are still not well understood, and its impact on neurons remains unclear. As a developmental outpocketing of the forebrain, the retina is a bellwether and model for damage to the central nervous system (CNS). In the rodent eye, astrocytes remain tightly restricted to a single layer on the inner retinal surface, beside a single layer of retinal ganglion cell neurons. This relatively simple system provides an accessible model of glial‐neuronal interactions. We have used the retina to develop and establish robust models of astrocyte activation in response to oxidative, metabolic, and hypoxic stresses. Characteristic molecular and biochemical changes in activated cells have implicated signals through the p38 MAPK (mitogen activated protein kinase) pathway as a key mediator of this process. We demonstrate that modulation of this pathway is necessary for the cells to mount an appropriate injury response. However, quiescent cells produce a neuroprotective effect on retinal neurons, while activated cells exacerbate injury.