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

作者：Yu, Li; Han, Ning; Jiang, Ligang; Zheng, Yajuan^*; Liu, Lifeng

来源：Neural Regeneration Research, 2011, 6(6): 450-456.

DOI：10.3969/j.issn.1673-5374.2011.06.009

• apoptosis
• CIC-3
• neuroprotection
• retinal ganglion cells
• Smads
• transforming growth factor

Transforming growth factor beta 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 beta 2, 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 beta/Smads signal transduction pathways are involved in this process.

• 出版日期2011-2-25
• 单位北华大学; 吉林大学