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Neuronal autophagy in cerebral ischemia

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Neuroscience Bulletin 2012年第5期28卷 658-666页

作者： Feng Xu Jin-Hua Gu Zheng-Hong Qin Department of Neurosurgery Huashan Hospital Fudan University Shanghai 200040 China Department of Pharmacology Nantong University School of Medicine Nantong 226001 China Department of Pharmacology and laboratory of aging and nervous diseases Soochow University School of Pharma-ceutical Science Suzhou 215123 China

Autophagy has evolved as a conserved process for the bulk degradation and recycling of cytosolic components, such as long-lived proteins and organelles. In neurons, autophagy is important for homeostasis and protein quality control and is maintained at relatively low levels under normal conditions, while it is upregulated in response to pathophysiological conditions, such as cerebral ischemic injury. However, the role of autophagy is more complex. It depends on age or brain maturity, region, severity of insult, and the stage of ischemia. Whether autophagy plays a beneficial or a detrimental role in cerebral ischemia depends on various pathological conditions. In this review, we elucidate the role of neuronal autophagy in cerebral ischemia.

关键词： autophagy cerebral ischemia neuron apoptosis necrosis

Hypermethylation in H3K9me3 regions characterizes the centenarian methylomes in healthy aging

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National Science Review 2023年第6期10卷 60-63页

作者： Fu-Hui Xiao Hao-Tian Wang Xiao-Qiong Chen Ming-Xia Ge Dongjing Yan Xing-Li Yang Li-Qin Yang Rong Lin Rong-Hui Guo Wen Zhang Nelson Leung-Sang Tang Yonghan He Jumin Zhou Wang-Wei Cai Qing-Peng Kong State Key laboratory of Genetic Resources and Evolution Key Laboratory of Healthy Aging Research of Yunnan Province Kunming Key Laboratory of Healthy Aging Study Kunming Institute of ZoologyChinese Academy of Sciences KIZ/CUHK Joint laboratory of Bioresources and Molecular Research in Common diseases Kunming College of Life Science University of Chinese Academy of Sciences Department of Biochemistry and Molecular Biology Hainan Medical College Department of Biology Hainan Medical College Department of Chemical Pathology and laboratory for Genetics of disease Susceptibility Li Ka Shing Institute of Health Sciences and School of Biomedical Sciences Faculty of Medicine The Chinese University of Hong Kong Key laboratory of Animal Models and Human disease Mechanisms of the Chinese Academy of Sciences Key Laboratory of Healthy Aging Research of Yunnan Province Kunming Institute of Zoology CAS Center for Excellence in Animal Evolution and Genetics Chinese Academy of Sciences

Centenarians,as excellent examples of extreme yet successful aging,not only display a much longer lifespan but can also delay or even escape major agerelated diseases,such as cardiovascular disorders,neurodegenerative diseases,and cancer [1].Studies have suggested that genetic factors account for 20%-30%of human longevity [2];however,only a handful of longevity-associated genes/mutations have been observed in long-lived individuals,even with the use of genome-wide scanning/sequencing assays [3,4].In contrast,evidence has shown the crucial roles of epigenetic alternations in aging and age-related diseases [5],suggesting that epigenetic modifications play central roles in human healthy ***,a comprehensive analysis of the epigenomic landscape of centenarians is urgently needed.

关键词： LONGEVITY DNA

Shenqi Fuzheng injection alleviates chemotherapy-induced cachexia by restoring glucocorticoid signaling in hypothalamus

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Journal of Pharmaceutical Analysis 2024年第3期14卷 431-434页

作者： Entezar Berik Zijia Zhang Wei Li Yawen Liu Sihan Chen Wenyong Wu Zhaojun Wang Xinqin Kong Wenqiang Pei Huiqing Dong Huali Long Min Lei Jennifer Yiyang Wang Liangfeng Liu Jinjun Hou Jing Feng Zhaoxia Li Wanying Wu De-an Guo Beijing Key Lab of TCM Collateral disease Theory Research School of Traditional Chinese MedicineCapital Medical UniversityBeijing100069China National Engineering Research Center of TCM Standardization Technology Shanghai Institute of Materia MedicaChinese Academy of SciencesShanghai201203China University of Chinese Academy of Sciences Beijing100049China School of Chinese Materia Medica Nanjing University of Chinese MedicineNanjing210029China Limin Pharmaceutical Factory Livzon Group LimitedShaoguanGuangdong512028China Guangdong Corporate Key laboratory of High-End Liquid Medicine R&D IndustrilizationShaoguanGuangdong512028China Center for Neurological and Psychiatric Research and Drug Discovery Shanghai Institute of Materia MedicaChinese Academy of ScienceShanghai201203China

Chemotherapy-induced cachexia(CIC)is a debilitating condition characterized by weight loss,muscle atrophy,and anorexia[1].While peripheral mechanisms of cachexia have been extensively studied,the involvement of the central nervous system(CNS)in CIC is often *** drugs cause stress responses and inflammation,which may impact the hypothalamus and disrupt systemic energy and neuroendocrine *** hypothalamic roles in regulating these processes can provide insights into CIC's mechanisms and aid in developing novel therapies.

关键词： injection drugs glucocorticoid chemotherapy

Infection with Listeria monocytogenes meningoencephalitis:A case report

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World Journal of Clinical Cases 2024年第33期12卷 6629-6634页

作者： Da-Zhen Xu Quan-Hui Tan Department of Nursing Shanghai Sixth People’s HospitalShanghai 200233China Department of Infectious disease Shanghai Sixth People’s HospitalShanghai 200233China

BACKGROUND Listeria meningitis is an infectious disease of the central nervous system caused by Listeria *** bacterium is widely present in the natural environment and can be transmitted through channels such as food and *** usually show symptoms such as fever,headache,and neck *** severe cases,coma,convulsions,or even death may *** diagnostic methods,such as cerebrospinal fluid(CSF)culture and serological tests,have certain *** CSF culture is the“gold standard”for diagnosis,it is time-consuming and has a relatively low positivity *** detection may also result in false positive or false negative *** emergence of metagenomic sequencing(mNGS)technology has led to a significant break-through in diagnosing Listeria meningitis,allowing quick and accurate detection of various pathogens in *** SUMMARY Here,we present the case of a previously healthy 64-year-old woman diagnosed with Listeria meningitis using *** was successfully treated with intravenous ampicillin and meropenem,without any *** Listeria meningitis must be considered,especially in patients who fail to show improvement with first-line antibiotic *** significantly reduces the diagnosis time,supporting timely treatment of patients.

关键词： Listeria monocytogenes Meningitis Diagnosis Treatment Immune function Case report

Mutant alpha-synuclein and autophagy in PC12 cells

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Neural Regeneration Research 2011年第2期6卷 91-95页

作者： Kangyong Liu Chunfeng Liu Chuancheng Ren Yaping Yang Liwei Shen Xuezhong Li Fen Wang Zhenghong Qin Department of Neurology Fifth Hospital of Fudan University Shanghai 200240 China Department of Neurologyl Second Affiliated Hospital of Soochow University Suzhou 216005 Jiangsu Province China laboratory of aging and'nervous diseases Soochow University Suzhou 216005 Jiangsu Province China

Several studies have demonstrated that overexpression of mutant a-synuclein in PC12 cells is related to occurrence of autophagy. The present study established mutant α-synuclein （A30P） -transfected PC12 cells and treated them with the autophagy inducer rapamycin and autophagy inhibitor wortmannin, respectively. Results demonstrated that mutant a-synuclein resulted in cell death via autophagy and involved a-synuclein accumulation, membrane lipid oxidation, and loss of plasma membrane integrity. Mutant a-synuclein （A30P） also mediated toxicity of 1-methyl-4-phenylpyridinium ion. Moreover, rapamycin inhibited a-synuclein aggregation, while wortmannin promoted α-synuclein aggregation and cell death. To further determine the role of autophagy due to mutant α-synuclein, the present study measured expression of microtubule-associated protein light chain 3. Results revealed that wortmannin and 1-methyl-4-phenylpyridinium ion inhibited expression of microtubule-associated protein light chain 3 while rapamycin promoted its expression. These findings suggested that abnormal aggregation of a-synuclein induced autophagic programmed cell death in PC12 cells.

关键词： α-synuclein autophagy microtubule-associated protein light chain 3 Parkinson's disease: PC12 cells

A Spleen Tyrosine Kinase’s Sky in Neuronal Degeneration

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Neuroscience Bulletin 2024年第2期40卷 273-276页

作者： Wan-Yun Zhang Sen Lin Department of Neurology Xinqiao HospitalThe Second Afliated HospitalArmy Medical UniversityChongqing 400042China Chongqing Institute for Brain and Intelligence Guangyang Bay LaboratoryChongqing 400064China

With the growing elderly population,neurodegenerative disorders like Alzheimer's disease(AD)are emerging as a significant public health *** is widely acknowledged in the scientific community that the accumulation of neurotoxic aggregates,such as amyloid beta(Aβ),within the central nervous system is a major factor in the development of these ***,human genome-wide association studies have identified mutations in microglial receptors that may be linked to a number of neurodegenerative diseases[1].

关键词： Aβ Spleen Alzheimer

SNX14 deficiency-induced defective axonal mitochondrial transport in Purkinje cells underlies cerebellar ataxia and can be reversed by valproate

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National Science Review 2021年第7期8卷 72-85页

作者： Hongfeng Zhang Yujuan Hong Weijie Yang Ruimin Wang Ting Yao Jian Wang Ke Liu Huilong Yuan Chaoqun Xu Yuanyuan Zhou Guanxian Li Lishan Zhang Hong Luo Xian Zhang Dan Du Hao Sun Qiuyang Zheng Yun-Wu Zhang Yingjun Zhao Ying Zhou Huaxi Xu Xin Wang State Key laboratory of Cellular Stress Biology Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research Institute of Neuroscience School of Medicine Xiamen University National Institute for Data Science in Health and Medicine School of Medicine Xiamen University Cancer Research Center Department of Stomatology School of Medicine Xiamen University

Loss-of-function mutations in sorting nexin 14(SNX14) cause autosomal recessive spinocerebellar ataxia20, which is a form of early-onset cerebellar ataxia that lacks molecular mechanisms and mouse models. We generated Snx14-deficient mouse models and observed severe motor deficits and cell-autonomous Purkinje cell degeneration. SNX14 deficiency disrupted microtubule organization and mitochondrial transport in axons by destabilizing the microtubule-severing enzyme spastin, which is implicated in dominant hereditary spastic paraplegia with cerebellar ataxia, and compromised axonal integrity and mitochondrial function. Axonal transport disruption and mitochondrial dysfunction further led to degeneration of highenergy-demanding Purkinje cells, which resulted in the pathogenesis of cerebellar ataxia. The antiepileptic drug valproate ameliorated motor deficits and cerebellar degeneration in Snx14-deficient mice via the restoration of mitochondrial transport and function in Purkinje cells. Our study revealed an unprecedented role for SNX14-dependent axonal transport in cerebellar ataxia, demonstrated the convergence of SNX14 and spastin in mitochondrial dysfunction, and suggested valproate as a potential therapeutic agent.

关键词： sorting nexin 14 cerebellar ataxia Purkinje cell degeneration mitochondrial dysfunction axonal transport valproate

Fasudil-modified macrophages reduce inflammation and regulate the immune response in experimental autoimmune encephalomyelitis

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Neural Regeneration Research 2024年第3期19卷 671-679页

作者： Chunyun Liu Shangde Guo Rong Liu Minfang Guo Qing Wang Zhi Chai Baoguo Xiao Cungen Ma Institute of Brain Science Shanxi Datong UniversityDatongShanxi ProvinceChina The Key Research laboratory of Benefiting Qi for Acting Blood Cireulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine/Research Center of Neurobiology Shanxi University of Chinese MedicineTaiyuanShanxi ProvinceChina Institute of Neurology Huashan HospitalInstitutes of Brain Science and State Key Laboratory of Medical NeurobiologyFudan UniversityShanghaiChina

Multiple sclerosis is characterized by demyelination and neuronal loss caused by inflammatory cell activation and infiltration into the central nervous *** polarization plays an important role in the pathogenesis of experimental autoimmune encephalomyelitis,a traditional experimental model of multiple *** study investigated the effect of Fasudil on macrophages and examined the therapeutic potential of Fasudil-modified macrophages in experimental autoimmune *** found that Fasudil induced the conversion of macrophages from the pro-inflammatory M1 type to the anti-inflammatory M2 type,as shown by reduced expression of inducible nitric oxide synthase/nitric oxide,interleukin-12,and CD16/32 and increased expression of arginase-1,interleukin-10,CD14,and CD206,which was linked to inhibition of Rho kinase activity,decreased expression of toll-like receptors,nuclear factor-κB,and components of the mitogen-activated protein kinase signaling pathway,and generation of the pro-inflammatory cytokines tumor necrosis factor-α,interleukin-1β,and ***,Fasudil-modified macrophages effectively decreased the impact of experimental autoimmune encephalomyelitis,resulting in later onset of disease,lower symptom scores,less weight loss,and reduced demyelination compared with unmodified *** addition,Fasudil-modified macrophages decreased interleukin-17 expression on CD4^(+)T cells and CD16/32,inducible nitric oxide synthase,and interleukin-12 expression on F4/80^(+)macrophages,as well as increasing interleukin-10 expression on CD4^(+)T cells and arginase-1,CD206,and interleukin-10 expression on F4/80^(+)macrophages,which improved immune regulation and reduced *** findings suggest that Fasudil-modified macrophages may help treat experimental autoimmune encephalomyelitis by inducing M2 macrophage polarization and inhibiting the inflammatory response,thereby providing new insight into cell immunotherapy for m

关键词： anti-inflammatory experimental autoimmune encephalomyelitis Fasudil macrophage multiple sclerosis pro-inflammatory Rho kinase

整合素α6靶向自组装促凋亡纳米多肽对中枢神经系统急性淋巴细胞白血病的靶向治疗

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Engineering 2024年第4期35卷 226-240页

作者： Jia-Cong Ye Wan-Qiong Li Mei-Ling Chen Qian-Kun Shi Hua Wang Xin-Ling Li Ying-He Li Jie Yang Qiao-Li Wang Fang Hu Yan-Feng Gao Shu-Wen Liu Mu-Sheng Zeng Guo-Kai Feng Guangdong Provincial Key laboratory of New Drug Screening&NMPA Key laboratory of Drug Metabolism Research and Evaluation School of Pharmaceutical SciencesSouthern Medical UniversityGuangzhou 510515China State Key laboratory of Oncology in South China&Guangdong Key laboratory of Nasopharyngeal Carcinoma Diagnosis and Therapy Guangdong Provincial Clinical Research Center for CancerSun Yat-sen University Cancer CenterGuangzhou 510060China School of Pharmaceutical Sciences(Shenzhen) Shenzhen Campus of Sun Yat-sen UniversityShenzhen 518107China Guangdong Provincial Key laboratory of Construction and Detection in Tissue Engineering Biomaterials Research CenterSchool of Biomedical EngineeringSouthern Medical UniversityGuangzhou 510515China State Key laboratory of Organ Failure Research Guangdong Provincial Institute of NephrologySouthern Medical UniversityGuangzhou 510515China

There is currently no effective targeted therapeutic strategy for the treatment of central nervous system acute lymphoblastic leukemia(CNS-ALL).Integrinα6 is considered a potential target for CNS-ALL diagnosis and therapy because of its role in promoting CNS-ALL disease *** targeted peptide D(RWYD)(abbreviated RD),with nanomolar affinity to integrinα6 was identified by peptide scanning techniques such as alanine scanning,truncation,and ***,we developed a therapeutic nanoparticle based on the integrinα6-targeted peptide for treating *** self-assembled proapoptotic nanopeptide_(D)(RWYD)-_(D)(KLAKLAK)_(2)-G_(D)(FFY)(abbreviated RD-KLA-Gffy)contains the integrinα6-targeted peptide RD,the well-known proapoptotic peptide_(D)(KLAKLAK)_(2)(abbreviated KLA),and the self-assembling tetrapeptide GD(FFY)(abbreviated Gffy).The functional mechanism of RD-KLA-Gffy is clarified using different *** results demonstrate that RD-KLA-Gffy is highly enriched in CNS-ALL lesions and induces tumor cell apoptosis,thus reducing CNS-ALL disease burden and prolonging the survival of CNS-ALL mice without obvious ***,the combined use of RD-KLA-Gffy and methotrexate(MTX)shows a potent antitumor effect in treating CNS-ALL,indicating that RD-KLA-Gffy plays an important role in suppressing CNS-ALL progression either as a single agent or in combination with MTX,which shows promise for application in CNS-ALL therapy.

关键词： Central nervous system acute lymphoblastic leukemia Integrinα6 Targeted peptide Proapoptotic Nanopeptide