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骨髓间充质干细胞来源的微囊泡通过 PI3K/Akt 依赖途径保护大鼠嗜铬细胞瘤 PC12 细胞免受谷氨酸诱导的损伤。

Bone marrow mesenchymal stem cell-derived microvesicles protect rat pheochromocytoma PC12 cells from glutamate-induced injury via a PI3K/Akt dependent pathway.

机构信息

Department of Rehabilitation Medicine, Zhujiang Hospital, Southern Medical University, 253 Gongye Road, Guangzhou, 510282, China.

出版信息

Neurochem Res. 2014 May;39(5):922-31. doi: 10.1007/s11064-014-1288-0. Epub 2014 Apr 6.

Abstract

Studies have suggested that mesenchymal stem cells (MSCs) can protect neuronal cells from excitotoxicity, but the underlying mechanisms are still remaining elusive. In the study, we show that microvesicles released by rat bone marrow-derived MSCs (rBMSC-MVs) protect rat pheochromocytoma PC12 cells from glutamate-induced excitotoxicity. BMSC-MVs upregulate Akt phosphorylation and Bcl-2 expression, downregulate Bax expression, and reduce the cleavage of caspase-3 in glutamate-treated PC12 cells. Such protective effects are partially abrogated by inhibiting PI3K, indicating that rBMSC-MVs act via the PI3K/Akt pathway. Transplantation of rBMSC-MVs may, therefore, be a promising strategy to treat cerebral injury or some other neuronal diseases involving excitotoxicity.

摘要

研究表明间充质干细胞(MSCs)可以保护神经元细胞免受兴奋毒性的损伤,但潜在的机制仍难以捉摸。在本研究中,我们发现大鼠骨髓来源的间充质干细胞(rBMSC-MVs)释放的微囊泡可以保护大鼠嗜铬细胞瘤 PC12 细胞免受谷氨酸诱导的兴奋毒性损伤。BMSC-MVs 上调 Akt 磷酸化和 Bcl-2 表达,下调 Bax 表达,并减少谷氨酸处理的 PC12 细胞中 caspase-3 的切割。通过抑制 PI3K,这种保护作用部分被阻断,表明 rBMSC-MVs 通过 PI3K/Akt 途径发挥作用。因此,rBMSC-MVs 的移植可能是治疗涉及兴奋毒性的脑损伤或其他一些神经元疾病的有前途的策略。

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