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Cyclophilin D-induced mitochondrial impairment confers axonal injury after intracerebral hemorrhage in mice

Neural Regeneration Research 2023年第4期18卷 849-855页

作者： Yang Yang Kai-Yuan Zhang Xue-Zhu Chen Chuan-Yan Yang Ju Wang Xue-Jiao Lei Yu-Lian Quan Wei-Xiang Chen Heng-Li Zhao Li-Kun Yang Yu-Hai Wang Yu-Jie Chen Hua Feng Department of Neurosurgery The 904th Hospital of PLAAnhui Medical UniversityWuxiJiangsu ProvinceChina Department of Neurosurgery and State Key Laboratory of Trauma Burn and Combined InjurySouthwest HospitalThird Military Medical University(Army Medical University)ChongqingChina Chongqing Key Laboratory of Precision Neuromedicine and Neuroregenaration Third Military Medical University(Army Medical University)ChongqingChina Wuxi Translational Medicine Center WuxiJiangsu ProvinceChina Department of Neurosurgery General Hospital of Xinjiang Military Command of PLAUrumqiXinjiang Uygur Autonomous RegionChina Department of Neurology The Second Medical Center&National Clinical Research Center for Geriatric DiseasesChinese PLA General HospitalBeijingChina

The mitochondrial permeability transition pore is a nonspecific transmembrane channel.Inhibition of mitochondrial permeability transition pore opening has been shown to alleviate mitochondrial swelling,calcium overload,and axonal degeneration.Cyclophilin D is an important component of the mitochondrial permeability transition pore.Whether cyclophilin D participates in mitochondrial impairment and axonal injury after intracerebral hemorrhage is not clear.In this study,we established mouse models of intracerebral hemorrhage in vivo by injection of autologous blood and oxyhemoglobin into the striatum in Thy1-YFP mice,in which pyramidal neurons and axons express yellow fluorescent protein.We also simulated intracerebral hemorrhage in vitro in PC12 cells using oxyhemoglobin.We found that axonal degeneration in the early stage of intracerebral hemorrhage depended on mitochondrial swelling induced by cyclophilin D activation and mitochondrial permeability transition pore opening.We further investigated the mechanism underlying the role of cyclophilin D in mouse models and PC12 cell models of intracerebral hemorrhage.We found that both cyclosporin A inhibition and short hairpin RNA interference of cyclophilin D reduced mitochondrial permeability transition pore opening and mitochondrial injury.In addition,inhibition of cyclophilin D and mitochondrial permeability transition pore opening protected corticospinal tract integrity and alleviated motor dysfunction caused by intracerebral hemorrhage.Our findings suggest that cyclophilin D is used as a key mediator of axonal degeneration after intracerebral hemorrhage;inhibition of cyclophilin D expression can protect mitochondrial structure and function and further alleviate corticospinal tract injury and motor dysfunction after intracerebral hemorrhage.Our findings provide a therapeutic target for preventing axonal degeneration of white matter injury and subsequent functional impairment in central nervous diseases.

关键词： axonal injury corticospinal tract cyclophilin D cyclosporin A intracerebral hemorrhage mitochondrial impairment mitochondrial permeability transition pore motor dysfunction retraction bulb white matter

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NLRP3 Inflammasome-Mediated Neuroinflammation and Related mitochondrial impairment in Parkinson's

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Neuroscience Bulletin 2023年第5期39卷 832-844页

作者： Qiu-Qin Han Weidong Le Shanghai University of Medicine and Health Sciences Affiliated Zhoupu Hospital Shanghai 201318China Center for Clinical and Translational Medicine Shanghai University of Medicine and Health SciencesShanghai 201318China

Parkinson's disease(PD)is a common neuro-degenerative disorder caused by the loss of dopamine neu-rons in the substantia nigra and the formation of Lewy bod-ies,which are mainly composed of alpha-synuclein fibrils.Alpha-synuclein plays a vital role in the neuroinflamma-tion mediated by the nucleotide-binding oligomerization domain-,leucine-rich repeat-,and pyrin domain-containing protein 3(NLRP3)inflammasome in PD.A better under-standing of the NLRP3 inflammasome-mediated neuroin-flammation and the related mitochondrial impairment during PD progression may facilitate the development of promis-ing therapies for PD.This review focuses on the molecular mechanisms underlying NLRP3 inflammasome activation,comprising priming and protein complex assembly,as well as the role of mitochondrial impairment and its subsequent inflammatory effects on the progression of neurodegenera-tion in PD.In addition,the therapeutic strategies targeting the NLRP3 inflammasome for PD treatment are discussed,including the inhibitors of NLRP3 inflammatory pathways,mitochondria-focused treatments,microRNAs,and other therapeutic compounds.

关键词： Parkinson's disease NLRP3 inflammasome Neuroinflammation mitochondrial impairment Microglia

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