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| 1 | Stress increases MHC-I expression in dopaminergic neurons and induces autoimmune activation in Parkinson’s disease显示文摘The expression of major histocompatibility complex class I(MHC-I),a key antigen-presenting protein,can be induced in dopaminergic neurons in the substantia nigra,thus indicating its possible involvement in the occurrence and development of Parkinson’s disease.However,it remains unclear whether oxidative stress induces Parkinson’s disease through the MHC-I pathway.In the present study,polymerase chain reaction and western blot assays were used to determine the expression of MHC-I in 1-methyl-4-phenylpyridinium(MPP+)-treated SH-SY5Y cells and a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP)-induced Parkinson’s disease mouse model.The findings revealed that MHC-I was expressed in both models.To detect whether the expression of MHC-I was able to trigger the infiltration of cytotoxic T cells,immunofluorescence staining was used to detect cytotoxic cluster of differentiation 8(CD8)+T cell infiltration in the substantia nigra of MPTP-treated mice.The results indicated that the presentation of MHC-I in dopaminergic neurons was indeed accompanied by an increase in the number of CD8+T cells.Moreover,in MPTP-induced Parkinson’s disease model mice,the genetic knockdown of endogenous MHC-I,which was caused by injecting specific adenovirus into the substantia nigra,led to a significant reduction in CD8+T cell infiltration and alleviated dopaminergic neuronal death.To further investigate the molecular mechanisms of oxidative stress-induced MHC-I presentation,the expression of PTEN-induced kinase 1(PINK1)was silenced in MPP+-treated SH-SY5Y cells using specific small interfering RNA(siRNA),and there was more presentation of MHC-I in these cells compared with control siRNA-treated cells.Taken together,MPP+-/MPTP-induced oxidative stress can trigger MHC-I presentation and autoimmune activation,thus rendering dopaminergic neurons susceptible to immune cells and degeneration.This may be one of the mechanisms of oxidative stress-induced Parkinson’s disease,and implies the potential neuroprotective role of PINK1 in oxidative stress-induced MHC-I presentation.All animal experiments were approved by the Southern Medical University Ethics Committee(No.81802040,approved on February 25,2018). | Bao-Yan Wang Yong-Yi Ye Chen Qian Hong-Bo Zhang Heng-Xu Mao Long-Ping Yao Xiang Sun Guo-Hui Lu Shi-Zhong Zhang | 2021 | Neural Regeneration Research2021，16，12： | 3 |
| 2 | 线粒体质量控制新途径:线粒体衍生囊泡显示文摘线粒体是真核细胞中非常复杂的双膜细胞器。在生理状态下,线粒体再生和降解是平衡的;细胞器中的蛋白质、脂质和DNA等组分受到损伤时,通过分裂、融合、自噬等途径维持线粒体稳态,以保持线粒体结构和功能的完整,这一过程通常称为'线粒体质量控制'。线粒体衍生囊泡(MDV)是新近发现的线粒体质量控制途径,在细胞应激早期有助于维持线粒体功能稳定,并在线粒体氧化应激中发挥重要作用。我们拟综述MDV的发现、转运途径、货物的选择以及对细胞的生理影响等。 | 官伟康 吕静 杨朝鲜 | 2021 | 解剖学报2021，52，1： | 1 |
| 3 | 蛋白激酶PINK1与炎症及免疫反应显示文摘磷酸酶及张力蛋白同源物诱导的蛋白激酶1(PTEN induced putative kinase 1,PINK1)是一种与线粒体自噬、帕金森病的发生发展密切相关的蛋白激酶。PINK1蛋白由581个氨基酸残基组成,具有高度保守的结构域,表达广泛。除了帕金森病,PINK1还参与多种疾病的发生、发展和调控,如肿瘤、糖尿病、心肺功能异常等。近年的研究表明,PINK1的表达影响T细胞的增殖和分化,抑制线粒体抗原递呈,参与调节机体固有免疫反应和炎症反应。另外,炎症小体NLRP3对肺内皮细胞的调节作用也与PINK1表达有关。PINK1也能通过NLRP3调节炎症介质的释放,参与脓毒症诱导的免疫代谢活动。本文就近年来PINK1与炎症、免疫反应的相关研究进行综述。 | 张召茹 周俊 | 2017 | 中国生物化学与分子生物学报2017，33，12： | 0 |
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