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

Neuroprotective effects of ClC-3 chloride channel in glutamate-induced retinal ganglion cell RGC-5 apoptosis
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摘要 Transforming growth factor β plays a role in regulation of apoptosis in CIC-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 CIC-3 cDNA-transfected glutamate-induced retinal ganglion cells. Following inhibition of the CIC-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 CIC-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. Transforming growth factor β plays a role in regulation of apoptosis in CIC-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 CIC-3 cDNA-transfected glutamate-induced retinal ganglion cells. Following inhibition of the CIC-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 CIC-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.
出处 《Neural Regeneration Research》 SCIE CAS CSCD 2011年第6期450-456,共7页 中国神经再生研究(英文版)
关键词 APOPTOSIS CIC-3 NEUROPROTECTION retinal ganglion cells SMADS transforming growth factor apoptosis CIC-3 neuroprotection retinal ganglion cells Smads transforming growth factor
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