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Neuroprotective effects of ClC-3 chloride channel in glutamate-induced retinal ganglion cell RGC-5 apoptosis

机译:ClC-3氯通道对谷氨酸诱导的视网膜神经节细胞RGC-5凋亡的神经保护作用

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摘要

Transforming growth factor β plays a role in regulation of apoptosis in ClC-3 and the Smads signaling pathway,although the underlying mechanisms remain unclear.The present study determined possible signal transduction mechanisms based on CIC-3 expression,which accordingly affected apoptosis of retinal ganglion cells in a glutamate-induced retinal ganglion cell RGC-5 apoptosis model.Results revealed significantly increased cell survival rate and significantly decreased apoptosis rate following apoptosis of ClC-3 cDNA-transfected glutamate-induced retinal ganglion cells.Following inhibition of the ClC-3 chloride channel using RNAi technology,cell survival and apoptosis rates were reversed.In addition,expression of transforming growth factor β2,Smads2,Smads3,Smads4,and Smads7 increased to varying degrees.These results suggest that ClC-3 chloride channel plays a protective role in glutamate-induced apoptosis of retinal ganglion cells,and transforming growth factor β/Smads signal transduction pathways are involved in this process.

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