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Editors Selection IGR 7-1

Basic research: Endothelin and astrocytes

Comment by Martin Wax on:

13731 Endothelin B receptor in human glaucoma and experimentally induced optic nerve damage, Wang L; Fortune B; Cull G et al., Archives of Ophthalmology, 2006; 124: 717-724

See also comment(s) by Rosario Hernandez •

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The interest in endothelins and glaucoma were originally limited to the area of vascular blood supply to the optic nerve over a decade ago. Endothelins are powerful vasoconstrictors, and several studies suggested that elevated endothelin-1 (ET-1) levels were detected in the aqueous humor from open-angle glaucoma patients and in the plasma of glaucoma patients, although the differences were relatively small compared to age-matched controls. Through the sustained efforts of the work in the Cioffi laboratory, a primate model of vascular insufficiency that may be relevant to glaucoma and perhaps other vascular insults such as Schnabel's cavernous optic atrophy has been developed that may help provide insights into mechanism of glaucomatous optic neuropathy. However, the role of endothelins in glaucoma pathogenesis is now receiving renewed attention, particularly in their role as potential mediators of astroglial activation that surely contributes, and possibly causes, optic nerve damage in glaucoma. Here, Wang et al. (454) examined the expression of endothelin receptors in human glaucomatous optic nerve.

The frequency of increased expression levels of endothelin B receptors is higher in glaucomatous optic nerves and the receptors were co-localized with reactive astrocyte processes

They showed that frequency of increased expression levels of endothelin B receptor (ETbR) was higher in human glaucomatous optic nerves as compared with age-matched controls. In addition, they showed that ETbR was colocalized with reactive astrocytic processes and was quantitatively higher in the human and monkey glaucomatous eyes. As seen in brain astrocytes subjected to trauma, the current findings suggest ET-1's role in astroglial activation under glaucomatous conditions. The increased ETbR in the processes of reactive astrocytes in the glaucomatous optic nerve provides evidence that astrocytes are involved in the pathological mechanisms of neuronal injury. However, additional work needs to be done to understand the precise mechanisms underlying the relationship between endothelins and astroglial activation. In glaucoma, the movement of selected components of anterograde axonal transport essential in ganglion cell survival appears to be impaired. Recent studies by Tom Yorio's group suggest that endothelin can in fact mediate inhibition of axonal transport (J Neurosci Res 2005; 79: 598-607; Invest Ophthalmol Vis Sci 2002; 43: 3223-3230). Thus, additional studies of endothelin receptors are certainly warranted as they could provide new insights in understanding the role of endothelins in pathogenesis of glaucoma.

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