In this week's Journal, Liu et al. provide some insight on what makes a "reactive" astrocyte reactive. The authors look at activated astrocytes using several models of optic nerve injury. The epidermal growth factor receptor (EGFR) was not expressed by quiescent astrocytes but was upregulated in rat optic nerve astrocytes after ischemia, nerve transection, and in a chronic glaucoma model. The authors used several approaches to examine EGFR signaling in astrocytes including microarray analysis and the analysis of motility of EGF-treated cultured astrocytes. Rats in a chronic glaucoma model were treated with the EGFR tyrosine kinase inhibitor AG1478 for 7 months. Untreated rats lost up to 20% of their retinal ganglion cells, whereas treated rats did not. In rats that went untreated for 3.5 months and then received AG1478, cell death was halted. The authors suggest that EGFR activation of astrocytes may play a detrimental role after injury.

Bin Liu, Huiyi Chen, Terrance G. Johns, and Arthur H. Neufeld

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