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Prof. Long Chen’s Group Obtained a Series of Achievements in Rapamycin’s Regulation of Cadmium-induced Neuronal Apoptosis/Neurodegeneration

Recently, Prof. Long Chen’s research group from College of Life Sciences in NNU obtained a series of achievements in rapamycin’s regulation of cadmium-induced neuronal apoptosis/neurodegeneration. Relevant achievements have been published on internationally renowned journals such as Neuropharmacology (2015; 97: 35-45; 2016; DOI: 10.1016/j.neuropharm. SCI IF=5.106) and Oncotarget (2015; 6: 21452-21467. SCI IF= 6.359) with the titles 'Rapamycin prevents cadmium-induced neuronal cell death via targeting both mTORC1 and mTORC2 pathways'; 'Rapamycin inhibits Erk1/2-mediated neuronal apoptosis caused by cadmium' and 'Rapamycin ameliorates cadmium-induced activation of MAPK pathway and neuronal apoptosis via suppressing mitochondrial ROS-inactivated PP2A', respectively. The first author of this series of papers is Chong Xu,a Ph.D student in the college, the total SCI IF is 16.57. 

Cadmium (Cd), a toxic heavy metal in environment, can accumulate in human body by food chain, and cause multi-organ toxicity. The studies have identified that Cd poisoning might be an important etiological factor of neurodegenerative diseases. Rapamycin, a macrocyclic lactone, is a clinical drug approved by US Food and Drug Administration (FDA). For the past few years, some studies have indicated that rapamycin has prolonged life and preventive effect on neurodegenerative diseases. Prof. Long Chen’s research group have explored the pathogenesis of Cd-induced neuronal apoptosis/neurodegenerative diseases via using the models of in vitro and in vivo Cd-induced neuronal apoptosis for years and obtained various outstanding achievements. This time, the group gained several breakthrough advances in investigating rapamycin’s prevention from Cd-induced neuronal apoptosis. Their findings are as follows : i) Rapamycin prevents Cd-induced neuronal apoptosis via targeting inhibition of mTORC1-mediated S6K1 and 4E-BP1 pathways, as well as mTORC2-mediated Akt pathway; ii) Rapamycin inhibits Cd-activated Erk1/2 against neuronal apoptosis via targeting PTEN/PP2A signaling network in an mTOR-dependent manner; iii). Rapamycin ameliorates Cd-induced neuronal apoptosis by preventing mitochondrial ROS mediation of PP2A-JNK/Erk1/2 pathway. These findings highlight that rapamycin provide important scientific basis and guidance as a promising agent for prevention of Cd-induced neuronal apoptosis and neurodegenerative disorders. 

The above series of studies are supported in part by the grants from National Natural Science Foundation of China, National Institutes of Health (NIH), Project for the Priority Academic Program Development of Jiangsu Higher Education Institutions of China (PAPD), Natural Science Foundation of Jiangsu Higher Education Institutions of China, and Innovative Research Program of Jiangsu College Graduate of China.