Abstract
Abstract: :
Purpose: To investigate the response of Müller cells in the early stages of ischemia– reperfusion injury. Methods: The intraocular pressure (IOP) was raised to 90–120 mmHg for 60 min, and the animals were sacrificed after 1 d, 3 d, 1 wk, 2 wk, and 4 wk of reperfusion. Immunocytochemistry using antisera against STAT 3, p–STAT 3 and ciliary neurotrophic factor (CNTF) or glutamine synthase (GS), a specific marker for Müller cell, were applied, and apoptotic cell death was determined by a modified TUNEL technique. Western blotting using anti–STAT 3 and p–STAT 3 antisera were applied, and double labeling using antisera against STAT 3, p–STAT 3 and GS or CNTF were performed. Results: STAT 3 and p–STAT 3 immunoreactivity was localized to most of all Müller cells. In addition, double labeling using antisera against STAT 3, p–STAT 3 and GS or CNTF demonstrated that these two antigens were expressed in same Müller cells. STAT 3 and p–STAT 3 labeled Müller cells did not show positive staining by TUNEL method. Conclusions: : Our findings demonstrate that most of Müller cells survive by STAT 3 pathway and suggest that STAT 3 produced and released by Müller cell may play an important role in the pathogenesis of ischemic injury in the rat retina.
Keywords: retina • retinal degenerations: cell biology • retinal glia