C-EBP Homologous Protein CHOP Deficiency Aggravates Hippocampal Cell Apoptosis and Impairs Memory PerformanceReport as inadecuate

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Neurodegenerative disorders are growing burdens in modern societies because of increased life expectancy. Most neurodegenerative disorders commonly possess a similar neuropathological feature - the accumulation of abnormal protein aggregates or inclusions misfolded proteins in the brain. One of the main functions of endoplasmic reticulum ER is to initiate proper protein folding to facilitate protein secretion through the induction of unfolded protein response UPR. C-EBP homologous protein CHOP induction has been demonstrated to be a signaling event underlying ER stress-induced cell apoptosis. In this study, we explored the role of CHOP in the hippocampal cell apoptosis and memory performance injury under an induced ER stress condition. Adult male wild type C57BL-6J and CHOP knockout CHOP−-− mice were intracerebroventricularly injected with tunicamycin. Tunicamycin can induce ER stress and cell apoptosis in mouse hippocampus. Compared with wild type mice, CHOP−-− mice showed an enhanced hippocampal cell apoptosis, worse performance in memory-related behavioral tests, and attenuated IRE-1 expression under tunicamycin treatment. The aggravated cell apoptosis and worse memory performance in CHOP−-− mice might be due to the deficiency of CHOP protein resulted in the impaired adaptive-pathological transcriptional response, the decreased IRE-1 and XBP-1 expressions, and the increased JNK phosphorylation to cope with ER stress. Taken together, these results suggest that CHOP may play a protective role in the hippocampal cell apoptosis and impairment of memory performance.

Author: Chang-Mu Chen , Cheng-Tien Wu, Chih-Kang Chiang, Bor-Wu Liao, Shing-Hwa Liu

Source: http://plos.srce.hr/


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