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Effects of the mitochondrial calcium uniporter on cerebral edema in a rat model of cerebral ischemia reperfusion injury

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Neural Regeneration Research 2011年第22期6卷 1720-1724页

作者： Linlin Li Shilei Wang Haihong Luan Department of Anesthesiology Affiliated Hospital of Qingdao University Medical College Qingdao 266003 Shandong Province China

The present study investigated the effects of the mitochondrial calcium uniporter inhibitor ruthenium red and the agonist spermine on cerebral edema in rats with cerebral ischemia reperfusion injury. Left middle cerebral artery occlusion （MCAO） was induced in rats using the suture method. Following 24 hours of ischemic reperfusion, neurological function scores of rats with MCAO, and rats pretreated with ruthenium red and spermine were significantly lower, however, water content of brain tissue, aquaporin 4 expression and immunoglobulin G （IgG） exudation were significantly higher than those of sham-operated rats. Compared with MCAO rats and spermine-treated rats, neurological function scores were considerably higher, and brain tissue water content, aquaporin 4 expression and IgG exudation decreased in ruthenium red-treated rats. These findings suggest that preventive application of the mitochondrial calcium uniporter inhibitor ruthenium red can significantly decrease aquaporin 4 and IgG expression, influence the permeability of the blood brain barrier, and thereby decrease the extent of cerebral edema.

关键词： cerebral ischemic reperfusion aquaporin 4 blood brain barrier brain edema mitochondrial calcium uniporter ruthenium red spermine neural regeneration

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An iron-dependent form of non-canonical ferroptosis induced by labile iron

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Science China(Life Sciences) 2023年第3期66卷 516-527页

作者： Yanmeng Li Qin Ouyang Wei Chen Ke Liu Bei Zhang Jingyi Yao Song Zhang Junying Ding Min Cong Anjian Xu Beijing Clinical Research Institute Beijing Friendship HospitalCapital Medical UniversityBeijing 100050China Beijing Key Laboratory of Basic Research with Traditional Chinese Medicine on Infectious Diseases Beijing Hospital of Traditional Chinese MedicineCapital Medical UniversityBeijing 100010China Liver Research Center Beijing Friendship HospitalCapital Medical UniversityBeijing 100050China

Ferroptosis is a recently identified iron-dependent form of nonapoptotic cell death characterized by reactive oxygen species(ROS) generation and lipid peroxidation.Here,we report a novel iron-dependent form of ferroptosis induced by labile iron and investigate the mechanism underlying this process.We find that labile iron-induced ferroptosis is distinct from canonical ferroptosis and is linked to the mitochondrial pathway.Specifically,the mitochondrial calcium uniporter mediates the ferroptosis induced by labile iron.Interestingly,cells undergoing labile iron-induced ferroptosis exhibit cytoplasmic features of oncosis and nuclear features of apoptosis.Furthermore,labile iron-induced ferroptosis involves a unique set of genes.Finally,labile ironinduced ferroptosis was observed in liver subjected to acute iron overload in vivo.Our study reveals a novel form of ferroptosis that may be implicated in diseases caused by acute injury.

关键词： ferroptosis labile iron calcium overload mitochondrial calcium uniporter cell death oncosis apoptosis

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Excitotoxicity, calcium and mitochondria: a triad in synaptic neurodegeneration

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Translational Neurodegeneration 2022年第1期11卷 917-930页

作者： Manish Verma Britney N.Lizama Charleen T.Chu Department of Pathology University of Pittsburgh School of MedicinePittsburghPA 15261USA Department of Ophthalmology University of Pittsburgh School of MedicinePittsburghPA 15261USA Pittsburgh Institute for Neurodegenerative Diseases University of Pittsburgh School of MedicinePittsburghPA 15261USA McGowan Institute for Regenerative Medicine University of Pittsburgh School of MedicinePittsburghPA 15261USA Center for Protein Conformational Diseases University of PittsburghPittsburghPA 15261USA Center for Neuroscience University of PittsburghPittsburghPA 15261USA Present Address:Astellas Pharma Inc. 9 Technology DriveWestboroughMA 01581USA.

Glutamate is the most commonly engaged neurotransmitter in the mammalian central nervous system,acting to mediate excitatory neurotransmission.However,high levels of glutamatergic input elicit excitotoxicity,contribut-ing to neuronal cell death following acute brain injuries such as stroke and trauma.While excitotoxic cell death has also been implicated in some neurodegenerative disease models,the role of acute apoptotic cell death remains controversial in the setting of chronic neurodegeneration.Nevertheless,it is clear that excitatory synaptic dysregula-tion contributes to neurodegeneration,as evidenced by protective effects of partial N-methyl-D-aspartate receptor antagonists.Here,we review evidence for sublethal excitatory injuries in relation to neurodegeneration associated with Parkinson’s disease,Alzheimer’s disease,amyotrophic lateral sclerosis and Huntington’s disease.In contrast to classic excitotoxicity,emerging evidence implicates dysregulation of mitochondrial calcium handling in excitatory post-synaptic neurodegeneration.We discuss mechanisms that regulate mitochondrial calcium uptake and release,the impact of LRRK2,PINK1,Parkin,beta-amyloid and glucocerebrosidase on mitochondrial calcium transporters,and the role of autophagic mitochondrial loss in axodendritic shrinkage.Finally,we discuss strategies for normalizing the flux of calcium into and out of the mitochondrial matrix,thereby preventing mitochondrial calcium toxicity and excitotoxic dendritic loss.While the mechanisms that underlie increased uptake or decreased release of mitochondrial calcium vary in different model systems,a common set of strategies to normalize mitochondrial calcium flux can prevent excitatory mitochondrial toxicity and may be neuroprotective in multiple disease contexts.

关键词： mitochondrial calcium mitochondrial calcium uniporter NCLX antiporter Parkinson’s disease Alzheimer’s disease LRRK2 PINK1 Beta-amyloid Mitophagy Excitotoxicity Amyotrophic lateral sclerosis Huntington’s disease Glucocerebrosidase

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