The neuroprotective roles of Muller cell in rat retinal ischemia-reperfusion injury

点击翻译按钮获取中文摘要

Purpose: We presented that the heat-shock proteins were expressed in Muller cells after rat retinal ischemia-reperfusion injury. To investigate the neuroprotective roles of Muller cells played in rat retinal ischemia-reperfusion injury by using the crystallin family short interfering RNA (siRNA).Methods: Retinal ischemia for 60 minutes was induced in rats by increasing the intraocular pressure to 110 mm Hg. The expression of 13E32-crystallin in the retina was determined by Western blot, real-time polymerase chain reaction (PCR), and immunohistochemistry. To inhibit the upregulation of βB2-crystallin, intravitreal injection of βB2-crystallin siRNA was performed before ischemia. The inhibition of Bβ2-crystallin expression was studied on Western blotting.Results: The expression of 6132-crystallin mRNA and protein were up-regulated at 6 hours after reperfusion and peaked at 12 hours. The βB2-crystallin immunoreactivities were detected in ganglion cells at 12 hours after reperfusion. The βB2-crystallin expression in the retina treated with siRNA of (βB2-crystallin was reduced at 12 hours after reperfusion compared with that injected with the control siRNA. On Western blotting, βB2-crystallin was downregulated at 12 hours after reperfusion. On TUNEL methods, the number of TUNEL positive cells in the ganglion cell layer and the internal nuclear layer reduced at 12 hours after ischemia-reperfusion injury. Conversely, αB-crystallin induced in Muller cell.Conclusions: pB2-crystallin may regulate the retinal ganglion cell death after ischemia-reperfusion injury. On the other hand, Muller cell might protect the ischemic retinal injuries due to αB-crystallin.