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CHCHD2 Thr61Ile mutation impairs F1F0-ATPase assembly in in vitro and in vivo models of Parkinson's disease

Neural Regeneration Research 2024年第1期19卷 196-204页

作者： Xiang Chen Yuwan Lin Zhiling Zhang Yuting Tang panghai ye Wei Dai Wenlong Zhang Hanqun Liu Guoyou Peng Shuxuan Huang Jiewen Qiu Wenyuan Guo Xiaoqin Zhu Zhuohua Wu Yaoyun Kuang Pingyi Xu Miaomiao Zhou Department of Neurology The First Affiliated Hospital of Guangzhou Medical UniversityGuangzhouGuangdong ProvinceChina Department of Neurology The People’s Hospital of Guangxi Zhuang Autonomous RegionNanningGuangxi Zhuang Autonomous RegionChina School of Basic Medical Sciences Guangzhou Medical UniversityGuangzhouGuangdong ProvinceChina Department of Neurology Shanghai General HospitalShanghai Jiao Tong University School of MedicineShanghaiChina

Mitochondrial dysfunction is a significant pathological alte ration that occurs in Parkinson's disease(PD),and the Thr61lle(T61I)mutation in coiled-coil helix coiled-coil helix domain containing 2(CHCHD2),a crucial mitochondrial protein,has been reported to cause Parkinson's ***-ATPase participates in the synthesis of cellular adenosine triphosphate(ATP)and plays a central role in mitochondrial energy ***,the specific roles of wild-type(WT)CHCHD2 and T611-mutant CHCHD2 in regulating F1FO-ATPase activity in Parkinson's disease,as well as whether CHCHD2 or CHCHD2 T61I affects mitochondrial function through regulating F1FO-ATPase activity,remain unclea ***,in this study,we expressed WT CHCHD2 and T61l-mutant CHCHD2 in an MPP^(+)-induced SH-SY5Y cell model of *** found that CHCHD2 protected mitochondria from developing MPP^(+)-induced *** normal conditions,ove rexpression of WT CHCHD2 promoted F1FO-ATPase assembly,while T61I-mutant CHCHD2 appeared to have lost the ability to regulate F1FO-ATPase *** addition,mass spectrometry and immunoprecipitation showed that there was an interaction between CHCHD2 and *** weeks after transfection with AAV-CHCHD2 T61I,we intraperitoneally injected 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine into mice to establish an animal model of chronic Parkinson's disease and found that exogenous expression of the mutant protein worsened the behavioral deficits and dopaminergic neurodegeneration seen in this *** findings suggest that WT CHCHD2 can alleviate mitochondrial dysfunction in PD by maintaining F1F0-ATPase structure and function.

关键词： ATP synthase(F1F0-ATPase) coiled-coil helix coiled-coil helix domain containing 2 dopaminergic neuron mitochondrial dysfunction neurodegeneration oligomycin sensitivity-conferring protein Parkinson's disease T61I mutation tyrosine hydroxylase

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Chaperone-mediated Autophagy Regulates Cell Growth by Targeting SMAD3 in Glioma

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Neuroscience Bulletin 2022年第6期38卷 637-651页

作者： Hanqun Liu Yuxuan Yong Xingjian Li panghai ye Kai Tao Guoyou Peng Mingshu Mo Wenyuan Guo Xiang Chen Yangfu Luo Yuwan Lin Jiewen Qiu Ziling Zhang Liuyan Ding Miaomiao Zhou Xinling Yang Lin Lu Qian Yang Pingyi Xu Department of Neurology The First Affliated Hospital of Guangzhou Medical UniversityGuangzhou 510120China Department of Neurosurgery Tangdu HospitalThe Fourth Military Medical UniversityXi'an 710038China Department of Neurology The Second Affliated Hospital of Xinjiang Medical UniversityUrimqi 830054China Department of Experiment Surgery Tangdu HospitalThe Fourth Military Medical UniversityXi'an 710038China

Previous studies suggest that the reduction of SMAD3(mothers against decapentaplegic homolog 3)has a great impact on tumor development,but its exact pathological function remains *** this study,we found that the protein level of SMAD3 was greatly reduced in human-grade IV glioblastoma tissues,in which LAMP2A(lysosome-associated membrane protein type 2A)was significantly ***2A is a key ratelimiting protein of chaperone-mediated autophagy(CMA),a lysosome pathway of protein degradation that is activated in *** carefully analyzed the amino-acid sequence of SMAD3 and found that it contained a pentapeptide motif biochemically related to KFERQ,which has been proposed to be a targeting sequence for *** vitro,we confirmed that SMAD3 was degraded in either serum-free or KFERQ motif deleted condition,which was regulated by LAMP2A and interacted with HSC70(heat shock cognate 71 kDa protein).Using isolated lysosomes,amino-acid residues 75 and 128 of SMAD3 were found to be of importance for this process,which affected the CMA pathway in which SMAD3 was ***,down-regulating SMAD3 or up-regulating LAMP2A in cultured glioma cells enhanced their proliferation and *** together,these results suggest that excessive activation of CMA regulates glioma cell growth by promoting the degradation of ***,targeting the SMAD3-LAMP2Amediated CMA-lysosome pathway may be a promising approach in anti-cancer therapy.

关键词： Glioma-SMAD3 Chaperone-mediated autophagy Cell growth

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旁海枢纽工程船闸输水系统布置及试验研究

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水运工程 2018年第12期 129-133页

作者：任启江叶雅思湖南省交通规划勘察设计院有限公司湖南长沙410000

高水头船闸常采用第二类输水系统以满足船闸闸室内水流条件的要求,但往往工程量大、施工复杂。根据船闸闸址处地形、地质条件,抬高闸底奠基高程以达到降低工程量并简化施工的目的,并在采取一定消能手段后,采用闸墙长廊道侧支孔输水形式... 详细信息

高水头船闸常采用第二类输水系统以满足船闸闸室内水流条件的要求,但往往工程量大、施工复杂。根据船闸闸址处地形、地质条件,抬高闸底奠基高程以达到降低工程量并简化施工的目的,并在采取一定消能手段后,采用闸墙长廊道侧支孔输水形式。通过物理模型,对旁海航电枢纽输水系统进行布置及优化,证实采取加大闸室初始淹没水深、闸室两侧出水口加设连续消力坎、优化进出水口布置及进水口布置帷墙等措施可达到预期效果。

关键词：高水头船闸输水系统闸墙长廊道侧支孔消能坎闸室初设淹没水深物理模型

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