PDZ结构域蛋白CAL缓解鱼藤酮引起的MN9D细胞损伤

来源 :中国生物化学与分子生物学报 | 被引量 : 0次 | 上传用户:a287924625
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PDZ(PSD95-DLG1-ZO1)域蛋白囊性纤维化跨膜电导调节相关配体(CAL)与Ⅰ组代谢型谷氨酸受体(m GluRⅠ)相互作用并且调节其下游信号.近年发现,m GluRⅠ与帕金森病密切相关.然而,CAL蛋白是否在帕金森病中发挥作用,目前尚未见报道.本文选用线粒体复合物Ⅰ抑制剂鱼藤酮处理小鼠多巴胺能神经元细胞系MN9D,建立帕金森病细胞模型,探讨CAL在鱼藤酮刺激多巴胺能神经元过程中的作用及可能机制.结果显示,鱼藤酮引起CAL蛋白表达减少,过表达CAL蛋白可以部分缓解鱼藤酮引起的MN9D细胞活力下降、细胞凋亡及c-Jun N端激酶(JNK)磷酸化.加入JNK抑制剂SP600125,鱼藤酮引起的细胞活力下降同样有所恢复.提示CAL蛋白可能通过调节JNK信号通路保护多巴胺能神经元. PDZ (PSD95-DLG1-ZO1) domain protein cystic fibrosis transmembrane conductance-dependent ligand (CAL) interact with and regulate the downstream signal of the group Ⅰ metabotropic glutamate receptor (m GluRⅠ) .In recent years, it was found that m GluR Ⅰ and Parkinson’s disease are closely related.However, CAL proteins play a role in Parkinson’s disease, has not been reported.This article selected mitochondrial complex Ⅰ inhibitor rotenone mouse dopaminergic neuronal cell line MN9D, the establishment of Parkinson’s disease Cell model to explore the role of CAL in the stimulation of dopaminergic neurons of rotenone and its possible mechanism.The results showed that rotenone caused a decrease of CAL protein expression and overexpression of CAL protein can partially alleviate the decline of rotenone-induced MN9D cell viability, apoptosis and c -Jun N-terminal kinase (JNK) phosphorylation.The JNK inhibitor SP600125 also restored the decline of cell viability induced by rotenone, suggesting that CAL protein may protect dopaminergic neurons by regulating the JNK signaling pathway.
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