Expression of ephrinB1 and its receptor in glaucomatous optic neuropathy
- 1Department of Ophthalmology, Northwestern University, Chicago, USA
- 2Department of Ophthalmology and Visual Sciences
- 3Department of Pediatrics, Washington University School of Medicine, St Louis, USA
- 4Department of Ophthalmology and Visual Sciences, University of Wisconsin Medical School, Madison, USA
- M Rosario Hernandez, Department of Ophthalmology, Northwestern University, 303 E. Chicago, Tarry, Chicago, USA;
- Accepted 4 February 2007
- Published Online First 14 February 2007
Objective: To determine ephrinB1, ephrinB2 and EphB1 expression in the optic nerve head (ONH) and retina of monkeys with glaucoma and in human ONH astrocytes.
Methods: Using immunohistochemistry, the localisation of ephrinB1, ephrinB2 and EphB1 was determined in the ONH and retina bilaterally in monkeys with monocular laser-induced glaucoma. RT-PCR, western blot and immunocytochemistry were used to study ephrinB1, ephrinB2 and EphB1 expression in cultured human ONH astrocytes from donors with and without glaucoma.
Results: There was an increase in ephrinB1 and EphB1 expression in mild to moderate glaucoma. In the ONH, both ephrinB1 and EphB1 were localised to astrocytes and EphB1 was also localised to lamina cribrosa cells and perivascular cells. In the retina, ephrinB1 localised to Muller cells and astrocytes, and EphB1 was found in retinal ganglion cells. In ONH astrocytes in humans with glaucoma, ephrinB1 and EphB1 were up-regulated but barely present in donors without glaucoma.
Conclusions: Ephrins are activated in early and moderate glaucoma in the ONH and retina. We postulate that the up-regulation of Eph/ephrin pathway may play a protective role by limiting axonal damage and inflammatory cell invasion. Loss of ephrin signalling in advanced glaucoma may explain macrophage activation.
This work was supported by NIH EY-06416 (MRH), and EY02698 (PLK), Research to Prevent Blindness, Ocular Physiology Research and Education Foundation, and Retina Research Foundation (Watler H Helmerich Chair).
Competing interests: None.
glial acidic fibrillar protein
National Disease Research Interchange
optic nerve head
primary open angle glaucoma
retinal ganglion cell