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Editors Selection IGR 11-4

Basic science: C-Fos and C-Jun and reactive astrocytes

Comment by James Lindsey on:

12548 Long-term activation of c-Fos and c-Jun in optic nerve head astrocytes in experimental ocular hypertension in monkeys and after exposure to elevated pressure in vitro, Hashimoto K; Parker A; Malone P et al., Brain Research, 2005; 1054: 103-115

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Glaucomatous optic nerve head tissue often contains substantial reactive astrocytes. These enlarged glia have increased cell surface molecules associated with cell-cell recognition, cell adhesion, and cell communication. However, little is known regarding changes in transcriptional regulation of gene expression in optic nerve head glia with glaucoma. Hashimoto et al. (831) address this issue by comparing the expression of five intracellular regulatory proteins in optic nerve head astrocytes in a variety of experimental settings. These included optic nerve head astrocytes within monkey eyes where intraocular pressure elevation had previously been induced by laser treatments, and cultured human astrocytes exposed to elevated hydrostatic pressure. They found increased nuclear expression of the transcription factors c-Fos and c-Jun in the reactive astrocytes from the monkey eyes with experimental glaucoma. This was similar to the increased expression of c-Fos and c-Jun within cultured human optic nerve head astrocytes exposed to increased hyrostatic pressure. They also observed increased expression of three upstream intracellular regulators that enhance activation of c-Fos and c-Jun in both settings. They concluded that induction of c-Fos and c-Jun may contribute to the formation of reactive astrocytes at the glaucomatous optic nerve head. The strengths of these experiments include straight forward experimental design, good attention to details during the induction of experimental intraocular pressure elevation, during the immunostaining protocols, during microscopy, and during quantitative analysis of the resulting images. However, this work does not determine what triggers the signaling cascades leading to c-Fos and c-Jun induction and astrocyte gliosis. Nevertheless, it does identify several signaling events that may be useful targets for the development of interventions to inhibit reactive astrocyte formation in glaucoma.

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