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Perilipin-2 mediates ferroptosis in oligodendrocyte progenitor cells and myelin injury after ischemic stroke

Neural Regeneration research 2025年第7期20卷 2015-2028页

作者： Jian Yang Jiang Wu Xueshun Xie Pengfei Xia Jinxin Lu Jiale Liu Lei Bai Xiang Li Zhengquan Yu Haiying Li Department of neurosurgery&brain and nerve research laboratory The First Affiliated Hospital of Soochow UniversitySuzhouJiangsu ProvinceChina Institute of Stroke research Soochow UniversitySuzhouJiangsu ProvinceChina

Differentiation of oligodendrocyte progenitor cells into mature myelin-forming oligodendrocytes contributes to *** of remyelination due to oligodendrocyte progenitor cell death can result in severe nerve *** is an iron-dependent form of regulated cell death caused by membrane rupture induced by lipid peroxidation,and plays an important role in the pathological process of ischemic ***,there are few studies on oligodendrocyte progenitor cell *** analyzed transcriptome sequencing data from GEO databases and identified a role of ferroptosis in oligodendrocyte progenitor cell death and myelin injury after cerebral *** analysis suggested that perilipin-2(PLIN2)was involved in oligodendrocyte progenitor cell ***2 is a lipid storage protein and a marker of hypoxia-sensitive lipid droplet *** further investigation,we established a mouse model of cerebral ischemia/*** found significant myelin damage after cerebral ischemia,as well as oligodendrocyte progenitor cell death and increased lipid peroxidation levels around the infarct *** ferroptosis inhibitor,ferrostatin-1,rescued oligodendrocyte progenitor cell death and subsequent myelin *** also found increased PLIN2 levels in the peri-infarct area that co-localized with oligodendrocyte progenitor ***2 knockdown rescued demyelination and improved neurological *** findings suggest that targeting PLIN2 to regulate oligodendrocyte progenitor cell ferroptosis may be a potential therapeutic strategy for rescuing myelin damage after cerebral ischemia.

关键词： bioinformatics bulk RNA sequencing ferroptosis ischemic stroke myelin injury oligodendrocyte progenitor cell perilipin-2 single-cell RNA sequencing

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Bioelectronic medicine in modulation of cortical spreading depolarization and beyond

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Neural Regeneration research 2025年第2期20卷 481-482页

作者： Khaled Alok Timothy G.White Chunyan Li Department of neurosurgery Donald and Barbara Zucker School of Medicine at Hofstra/NorthwellHempsteadNYUSA Translational brain research laboratory The Feinstein Institutes for Medical ResearchManhassetNYUSA

Bioelectronic interventions,specifically trigeminal nerve st imulat ion(TNS),have attracted considerable attention in conditions where cortical spreading depolarizations(CSDs)accompanied by compromised cerebral perfusion may exacerbate neurological *** pharmacological interventions have demonstrated initial potential in addressing CSDs,a standardized treatment approach has not yet been *** objective of this perspective is to explore emerging bioelectronic methodologies for addressing CSDs,particularly emphasizing TNS,and to underscore TNS’s capacity to enhance neurovascular coupling and cerebral perfusion.

关键词： cerebral perfusion electronic

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Glucocorticoid receptor signaling in the brain and its involvement in cognitive function

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Neural Regeneration research 2025年第9期20卷 2520-2537页

作者： Chonglin Su Taiqi Huang Meiyu Zhang Yanyu Zhang Yan Zeng Xingxing Chen brain Science and Advanced Technology Institute Hubei Province Key Laboratory of Occupational Hazard Identification and ControlSchool of MedicineWuhan University of Science and TechnologyWuhanHubei ProvinceChina

The hypothalamic-pituitary-adrenal axis regulates the secretion of glucoco rticoids in response to environmental *** the brain,a nuclear receptor transcription fa ctor,the glucocorticoid recepto r,is an important component of the hypothalamicpituitary-a d renal axis's negative feedback loop and plays a key role in regulating cognitive equilibrium and *** glucoco rticoid receptor influences cognitive processes,including glutamate neurotransmission,calcium signaling,and the activation of brain-derived neurotrophic factor-mediated pathways,through a combination of genomic and non-genomic *** interactions within the central nervous system can alter the expression and activity of the glucocorticoid receptor,there by affecting the hypothalamic-pituitary-a d renal axis and stress-related cognitive *** appropriate level of glucocorticoid receptor expression can improve cognitive function,while excessive glucocorticoid receptors or long-term exposure to glucoco rticoids may lead to cognitive *** with cognitive impairment-associated diseases,such as Alzheimer's disease,aging,depression,Parkinson's disease,Huntington's disease,stroke,and addiction,often present with dysregulation of the hypothalamic-pituitary-adrenal axis and glucocorticoid receptor *** review provides a comprehensive overview of the functions of the glucoco rticoid receptor in the hypothalamic-pituitary-a d renal axis and cognitive *** emphasizes that appropriate glucocorticoid receptor signaling fa cilitates learning and memory,while its dysregulation can lead to cognitive *** provides clues about how glucocorticoid receptor signaling can be targeted to ove rcome cognitive disability-related disorders.

关键词： brain-derived neurotrophic factor calcium signaling glucocorticoid receptor glucocorticoid glutamate transmission hypothalamic-pituitary-adrenal axis long-term potentiation neurocognitive disorders neuroplasticity stress

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Loss of monocarboxylate transporter 1 aggravates white matter injury after experimental subarachnoid hemorrhage in rats

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Frontiers of Medicine 2021年第6期15卷 887-902页

作者： Xin Wu Zongqi Wang Haiying Li Xueshun Xie Jiang Wu Haitao Shen Xiang Li Zhong Wang Gang Chen Department of neurosurgery&brain and nerve research laboratory The First Affiliated Hospital of Soochow UniversitySuzhou215006China

Monocarboxylic acid transporter 1(MCT1)maintains axonal function by transferring lactic acid from oligodendrocytes to *** hemorrhage(SAH)induces white matter injury,but the involvement of MCT1 is *** this study,the SAH model of adult male Sprague-Dawley rats was used to explore the role of MCT1 in white matter injury after *** 48 h after SAH,oligodendrocyte MCT1 was significantly reduced,and the exogenous overexpression of MCT1 significantly improved white matter integrity and long-term cognitive *** training after SAH significantly increased the number of ITPR2+SOX10+oligodendrocytes and upregulated the level of MCT1,which was positively correlated with the behavioral ability of *** addition,miR-29b and miR-124 levels were significantly increased in SAH rats compared with non-SAH *** intervention experiments showed that miR-29b and miR-124 could negatively regulate the level of *** study confirmed that the loss of MCT1 may be one of the mechanisms of white matter damage after SAH and may be caused by the negative regulation of miR-29b and ***1 may be involved in the neurological improvement of rehabilitation training after SAH.

关键词： microRNAs monocarboxylate transporter 1 motor training subarachnoid hemorrhage white matter injury

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High-dose dexamethasone regulates microglial polarization via the GR/JAK1/STAT3 signaling pathway after traumatic brain injury

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Neural Regeneration research 2025年第9期20卷 2611-2623页

作者： Mengshi Yang Miao Bai Yuan Zhuang Shenghua Lu Qianqian Ge Hao Li Yu Deng Hongbin Wu Xiaojian Xu Fei Niu Xinlong Dong Bin Zhang Baiyun Liu Beijing Tiantan Hospital Capital Medical UniversityBeijingChina Department of Neurology The First Hospital of Tsinghua UniversityBeijingChina Department of Neurotrauma and Beijing Key laboratory of Central Nervous System Injury Beijing Neurosurgical InstituteCapital Medical UniversityBeijingChina Department of Critical Care Medicine Beijing Tiantan HospitalCapital Medical UniversityBeijingChina Center for nerve Injury and Repair Beijing Institute of Brain DisordersChina National Clinical Research Center for Neurological DiseasesBeijingChina

Although microglial polarization and neuroinflammation are crucial cellular responses after traumatic brain injury,the fundamental regulatory and functional mechanisms remain insufficiently *** potent anti-inflammato ry agents,the use of glucoco rticoids in traumatic brain injury is still controversial,and their regulatory effects on microglial polarization are not yet *** the present study,we sought to determine whether exacerbation of traumatic brain injury caused by high-dose dexamethasone is related to its regulatory effects on microglial polarization and its mechanisms of *** vitro cultured BV2 cells and primary microglia and a controlled cortical impact mouse model were used to investigate the effects of dexamethasone on microglial ***,dexamethasone,RU486(a glucocorticoid receptor antagonist),and ruxolitinib(a Janus kinase 1 antagonist)were ***-sequencing data obtained from a C57BL/6 mouse model of traumatic brain injury were used to identify potential targets of *** Morris water maze,quantitative reverse transcription-polymerase chain reaction,western blotting,immunofluorescence and confocal microscopy analysis,and TUNEL,Nissl,and Golgi staining were performed to investigate our ***-throughput sequencing results showed that arginase 1,a marker of M2 microglia,was significantly downregulated in the dexamethasone group compared with the traumatic brain injury group at3 days post-traumatic brain *** dexamethasone inhibited M1 and M2 microglia,with a more pronounced inhibitory effect on M2microglia in vitro and in *** receptor plays an indispensable role in microglial polarization after dexamethasone treatment following traumatic brain ***,glucocorticoid receptor activation increased the number of apoptotic cells and neuronal death,and also decreased the density of dendritic spines.A possible downstream receptor signaling mechanism is th

关键词： apoptosis BV2 microglia dexamethasone glucocorticoid receptor glucocorticoids innate immune system microglial polarization neuroinflammation primary microglia traumatic brain injury

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Oestrogen ameliorates blood-brain barrier damage after experimental subarachnoid haemorrhage via the SHH pathway in male rats

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Stroke & Vascular Neurology 2023年第3期8卷 217-228,I0060-I0073页

作者： Jie Zhang Haiying Li Zhongmou Xu Jinxin Lu Chang Cao Haitao Shen Xiang Li Wanchun You Gang Chen Department of neurosurgery&brain and nerve research laboratory First Affiliated Hospital of Soochow UniversitySuzhouJiangsuChina Institute of Stroke research Soochow UniversitySuzhouChina

Background Sex differences affect the occurrence,progression and regression of subarachnoid haemorrhage(SAH).Oestrogen plays a protective role in alleviating the vasospasm and neuronal apoptosis induced by ***,whether oestrogen affects blood‒brain barrier(BBB)integrity has not been fully *** has been found to regulate the sonic hedgehog(SHH)signalling pathway through the oestrogen receptor in gastric cancer and adrenal glands,and the SHH signalling pathway has an important role in maintaining the BBB by upregulating the expression of tight junction *** this study,we investigated the relationship between oestrogen and the SHH signalling pathway using clinical data and established an experimental SAH model to explore whether oestrogen could ameliorate BBB damage after SAH through the SHH *** Correlations between oestrogen and the SHH pathway were analysed by patients’cerebrospinal fluid(CSF)samples and the Genotype-Tissue Expression database(GTEx).Then,an experimental rat SAH model was established using the endovascular perforation method and treated with oestrogen,oestrogen inhibitors and SHH signalling pathway ***,the effects of oestrogen on BBB damage were analysed by western blot,immunofluorescence and neurobehavioural *** ESLIA detection and correlation analysis showed that oestrogen levels in patients’CSF were positively correlated with the SHH pathway,which was further verified by GTEx gene-correlation *** was found to be mainly expressed in neurons and astrocytes in rats under physiological conditions and was upregulated by oestrogen *** the SAH model,oestrogen pretreatment was found to reverse SAH-induced decreases in the SHH pathway,which were counteracted by oestrogen receptor ***,oestrogen pretreatment reduced SAH-induced BBB damage,brain oedema and neurological dysfunction,which were eliminated by SHH pathway *** In conclusion,we

关键词： damage barrier SHH

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APE1 regulates mitochondrial DNA damage repair after experimental subarachnoid haemorrhage in vivo and in vitro

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Stroke & Vascular Neurology 2024年第3期9卷 230-242,I0133-I0209页

作者： Kun Dai Zongqi Wang Bixi Gao Longyuan Li Feng Gu Xinyu Tao Wanchun You Zhong Wang Department of neurosurgery&brain and nerve research laboratory First Affiliated Hospital of Soochow UniversitySuzhouJiangsuChina Institute of Stroke research Soochow UniversitySuzhouJiangsuChina

Background Subarachnoid haemorrhage(SAH)can result in a highly unfavourable *** recent years,the study of SAH has focused on early brain injury(EBI),which is a crucial progress that contributes to adverse *** can lead to various complications,including mitochondrial dysfunction and DNA ***/apyrimidinic endonuclease 1(APE1)is an essential protein with multifaceted functionality integral to DNA repair and redox ***,the role of APE1 in mitochondrial DNA damage repair after SAH is still *** Our study involved an in vivo endovascular perforation model in rats and an in vitro neuron oxyhaemoglobin ***,the effects of APE1 on mitochondrial DNA damage repair were analysed by western blot,immunofluorescence,quantitative real-time PCR,mitochondrial bioenergetics measurement and neurobehavioural *** We found that the level of APE1 decreased while the mitochondria DNA damage and neuronal death increased in a rat model of *** of APE1 improved short-term and long-term behavioural impairment in rats after *** vitro,after primary neurons exposed to oxyhaemoglobin,APE1 expression significantly decreased along with increased mitochondrial DNA damage,a reduction in the subunit of respiratory chain complex levels and subsequent respiratory chain *** of APE1 relieved energy metabolism disorders in the mitochondrial of neurons and reduced neuronal *** In conclusion,APE1 is involved in EBI after SAH by affecting mitochondrial apoptosis via the mitochondrial respiratory ***1 may potentially play a vital role in the EBI stage after SAH,making it a critical target for treatment.

关键词： APE1 damage vivo after

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Axonal mRNA localization and local translation in neurodegenerative diseases

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Neural Regeneration research 2021年第10期16卷 1950-1957页

作者： Jin-Xin Lu Yang Wang Yi-Jie Zhang Mei-Fen Shen Hai-Ying Li Zheng-Quan Yu Gang Chen Department of neurosurgery&brain and nerve research laboratory The First Affiliated Hospital of Soochow UniversitySuzhouJiangsu ProvinceChina Department of neurosurgery The First Affiliated Hospital of University of Science and Technology of ChinaHefeiAnhui ProvinceChina

The regulation of mRNA localization and local translation play vital roles in the maintenance of cellular structure and *** human neurodegenerative diseases,such as fragile X syndrome,amyotrophic lateral sclerosis,Alzheimer’s disease,and spinal muscular atrophy,have been characterized by pathological changes in neuronal axons,including abnormal mRNA translation,the loss of protein expression,or abnormal axon ***,the same protein and mRNA molecules have been associated with variable functions in different diseases due to differences in their interaction *** this review,we briefly examine fragile X syndrome,amyotrophic lateral sclerosis,Alzheimer’s disease,and spinal muscular atrophy,with a focus on disease pathogenesis with regard to local mRNA translation and axon transport,suggesting possible treatment directions.

关键词： Alzheimer’s disease amyotrophic lateral sclerosis axonal transport fragile X syndrome local translation mRNA localization neuron spinal muscular atrophy

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Differential distribution of PINK1 and Parkin in the primate brain implies distinct roles

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Neural Regeneration research 2025年第4期20卷 1124-1134页

作者： Yanting Liu Wei Huang Jiayi Wen Xin Xiong Ting Xu Qi Wang Xiusheng Chen Xianxian Zhao Shihua Li Xiaojiang Li Weili Yang Guangdong Key laboratory of Non-human Primate research Key Laboratory of CNS Regeneration(Ministry of Education)Guangdong-Hongkong-Macao CNS Regeneration Institute of Jinan UniversityJinan UniversityGuangzhouGuangdong ProvinceChina

The vast majority of in vitro studies have demonstrated that PINK1 phosphorylates Parkin to work together in mitophagy to protect against neuronal ***,it remains largely unclear how PINK1 and Parkin are expressed in mammalian *** has been difficult to address because of the intrinsically low levels of PINK1 and undetectable levels of phosphorylated Parkin in small *** this issue is critical for elucidating the in vivo roles of PINK1 and ***,we showed that the PINK1 kinase is selectively expressed as a truncated form(PINK1–55)in the primate *** the present study,we used multiple antibodies,including our recently developed monoclonal anti-PINK1,to validate the selective expression of PINK1 in the primate *** found that PINK1 was stably expressed in the monkey brain at postnatal and adulthood stages,which is consistent with the findings that depleting PINK1 can cause neuronal loss in developing and adult monkey ***1 was enriched in the membrane-bound fractionations,whereas Parkin was soluble with a distinguishable *** double staining experiments showed that PINK1 and Parkin did not colocalize under physiological conditions in cultured monkey astrocytes,though they did colocalize on mitochondria when the cells were exposed to mitochondrial *** findings suggest that PINK1 and Parkin may have distinct roles beyond their well-known function in mitophagy during mitochondrial damage.

关键词： neurodegeneration Parkin Parkinson’s disease PINK1 subcellular distribution

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Glial response in the midcingulate cortex in Huntington’s disease

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Neural Regeneration research 2025年第1期20卷 207-208页

作者： Thulani H.Palpagama Andrea Kwakowsky Center for brain research and Department of Anatomy and Medical Imaging Faculty of Medical and Health SciencesUniversity of AucklandAucklandNew Zealand Pharmacology and Therapeutics School of MedicineGalway Neuroscience CenterUniversity of GalwayGalwayIreland

Huntington’s disease(HD)is a genetic disease characterized by the progressive degeneration of the striatum and *** can present with a variety of symptoms that can broadly be classified into motor symptoms,inclusive of choreatic movements and rigidity,mood and psychiatric symptoms,such as depression and apathy,and cognitive symptoms,such as cognitive *** causal mutation underlying HD results from an expansion of a CAG repeat sequence on the IT15 gene,resulting in the formation and accumulation of a mutant huntingtin protein.

关键词： Huntington degeneration cortex

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