Purchase this article with an account.
W-K Ju, AH Neufeld; Differential Expression of Cyclooxygenase-1 and Cyclooxygenase-2 in the Rat Retina After Transient Ischemia . Invest. Ophthalmol. Vis. Sci. 2002;43(13):658.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
Purpose: Prostaglandins, synthesized by cyclooxygenase (COX), modulate inflammation, immune responses, blood flow, apoptosis and secondary injury in the ischemic brain. However, relatively little is known about prostaglandins in the neural retina after ischemia. We have determined the differential expression, time course and cellular localization of COX-1 and COX-2 in the rat retina after transient ischemia. Methods: Transient retinal ischemia was produced by controlled elevation of IOP above systolic blood pressure for 75 min in rats. By using immunohistochemistry and immunoblot analysis, we compared the cellular expression of COX-1 and COX-2 in the rat retina from 6 hours to 7 days after ischemia. Results: In the normal rat retina, COX-1 is present in retinal ganglion cells (RGCs), displaced amacrine cells and microglia in the outer plexiform layer (OPL), inner plexiform layer (IPL) and ganglion cell layer (GCL). In the ischemic rat retina, COX-1 immunoreactivity is sustained in microglia during the post-ischemia period. In neurons of the GCL, COX-1 immunoreactivity is diminished from 1 day after ischemia but is present in a few neuronal cells at 7 days after ischemia. Immunoblot for COX-1 demonstrates its presence in the retina of normal eyes and relative changes in the ischemic rat retina. In the normal rat retina, COX-2 is present in a few cells in the inner nuclear layer (INL). In the ischemic rat retina, COX-2 is significantly induced in the perinuclear region and the processes of Muller cells from 6 hours after ischemia. At 12 hours after ischemia, a few cells with large somas, that are likely to be RGCs, also express COX-2. From 3 days after ischemia, COX-2 positive cells are not present in the INL or GCL. However, COX-2 immunoreactivity is present in the processes of Muller cells in the IPL and GCL for 7 days after ischemia. Immunoblot for COX-2 demonstrates its faint presence in normal retinas. In the ischemic rat retina, COX-2 is significantly increased at 6 hours and peaks at 12 hours after ischemia. By immunoblot, the expression level of COX-2 decreases at 1 day and has almost disappeared at 3 days after ischemia. Conclusion: Prostaglandins, synthesized by constitutive COX-1 may play an important role in normal physiological functions of RGCs, displaced amacrine cells and microglia in the retina. COX-2, which is constitutive in a limited number of retinal cells, is rapidly induced in Muller cells after ischemia and may participate in early pathophysiological events.
This PDF is available to Subscribers Only