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Expression and regulation of versican in neural precursor cells and their lineages

Acta Pharmacologica Sinica 2007年第10期28卷 1519-1530页

作者： Wen-li GU~(2,3),Sai-li FU~2,Yan-xia WANG~2,Ying LI~2,Xiao-fei WANG~2,Xiao-ming XU~(2,4),Pei-hua LU~(2,5)~2 department of Neurobiology,Shanghai Jiao Tong university school of medicine,Shanghai 200025,China ~3 department of ClinicalLaboratory,Ninth People's Hospital of Shanghai,Shanghai Jiao Tong university,Shanghai 200011,China ~4 department of neurological surgery,university of louisville school of medicine,louisville,kentucky 40292,usa department of Neurobiology Shanghai Jiao Tong University School of Medicine Shanghai China department of Clinical Laboratory Ninth People's Hospital of Shanghai Shanghai Jiao Tong University Shanghai China department of neurological surgery University of Louisville School of Medicine Louisville USA

Aim:To have a better understanding of the expression and regulation of versicanisoforms in neural precursor cells (NPC) and ***:By immunocytochemistry,RT-PCR,and real-time PCR,we examined the tem-poral expression of versican in NPC isolated from embryonic d 16 rats as wellas in oligodendrocyte (OL) lineage cells induced to differentiate from NPC,which mimicked the oligodendrogliogenesis in ***:We found thatversican was constitutively expressed in NPC and their lineage cells,includingneurons,astrocytes,and *** addition,2 versican isoforms,V1/V0 and V2,were found to express at low levels in NPC,but at significantly higher levels inOL lineage *** peak expression of versican V2 was found at the oligo-dendrocyte precursor cell ***,the treatment of 2 pro-inflam-matory cytokines,TNF-α and IFN-γ,enhanced the transcription of versican V2in NPC in a dose-dependent manner,but showed no effect on V1/V0 ***:Taken together,our results demonstrate that versican,particularlythe inhibitory V2 isoform,is increasingly expressed in OL lineage cells inducedto differentiate from *** increase in versican V2 expression after cytokinestimulation implies the interplay between the injury-induced upregulation ofinflammatory cytokines and chondroitin sulfate proteoglycan-mediated inhibi-tion of axonal regeneration after central nervous system injury.

关键词： chondroitin sulfate proteoglycans neural precursor cells oligodendrocyte precursor cells oligodendrocytes pro-inflammatory cytokines versican

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Upregulation of heparin-binding growth-associated molecule after spinal cord injury in adult rats

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Acta Pharmacologica Sinica 2004年第5期25卷 69-74页

作者： Yan-ting WANG2, Shu HAN2, Kai-hua ZHANG2, Yu JIN3, Xiao-ming XU2,4, Pei-hua LU2,52department of Neurobiology, Shanghai Second Medical university, Shanghai 200025, China 3department of surgery,Xinhua Hospital Affiliated to Shanghai Second Medical university 4kentucky Spinal Cord Injury Research Center,department of neurological surgery, university of louisville school of medicine, louisville, KY, 40292, usa department of Neurobiology Shanghai Second Medical University 上海 200025

AIM: To investigate whether traumatic spinal cord injury (SCI) induces changes of gene expression of heparin-binding growth-associated molecule (HB-GAM). METHODS: In a spinal cord transection model, HB-GAM ex-pression and cellular localization were examined using Northern blot, RT-PCR, immunohistochemistry and immun-ofluorescence double-labeling methods. RESULTS: HB-GAM mRNA was significantly upregulated in spinal cordtissues rostral and caudal to the injury at 7 d after SCI. HB-GAM gene expression was markedly increased at 3 d,peaked at 7 d, and declined to the baseline level at 28 d post-injury. During its peak expression, HB-GAM was co-localized in astrocytes, oligodendrocytes, and neurons in spinal cord tissues within 7 mm from the site of spinaltransection. CONCLUSION: SCI induces HB-GAM expression at both mRNA and protein levels in areas close tothe injury. Both neurons and glial cells expressed HB-GAM implying that HB-GAM played a role in the process ofinjury and/or repair following SCI.

关键词： heparin-binding growth-associated molecule spinal cord injuries immunohistochemistry reversetranscriptase polymerase chain reaction astrocytes neurons

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Upregulation of S100A4 after spinal cord transectionin adult rats

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Acta Pharmacologica Sinica 2004年第8期 34-39页

作者： Kai-hua ZHANG, Shu HAN, Pei-hua LU, Xiao-ming XUdepartment of Neurobiology, Shanghai Second Medical university, Shanghai 200025, China kentucky Spinal Cord Injury Research Center, department of neurological surgery and Anatomical Sciencesand Neurobiology, university of louisville school of medicine, louisville, KY 40292, usa

AIM: To investigate whether spinal cord transection induces changes of gene expression of S100A4 protein. METHODS: In a spinal cord transection model, S100A4 expression and cellular localization were examined using cDNA microarray, Northern blot, immunohistochemistry, and immunofluorescence double-labeling methods. RESULTS: There was very limited S100A4 mRNA expression in the control spinal cord. However, S100A4 mRNA expression was increased significantly in both the rostral and caudal spinal cord segments adjacent to the injury site. Specifically, S100A4 gene expression was substantially increased at d 2, peaked at d 7 and d 14, and remained high up to 28 d post-injury. During its peak expression, S100A4 protein was localized in astrocytes of the spinal cord within 5 mm from the site of spinal transection. CONCLUSION: Spinal cord transection induces prolonged S100A4 expression at both mRNA and protein levels in areas close to the injury site. Increased expression of S100A4 in astrocytes after spinal cor

关键词： spinal cord injury S100A4 gene expression

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Effects of annexins II and V on survival of neurons and astrocytes in υitro

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Acta Pharmacologica Sinica 2004年第5期 60-68页

作者： Shu HAN2, Kai-hua ZHANG2, Pei-hua LU2,3, Xiao-ming XU2,3,42department of Neurobiology, Shanghai Second Medical university, Shanghai 200025, China4kentucky Spinal Cord Injury Research Center, department of neurological surgery,university of louisville school of medicine, louisville, KY 40292,usa

AIM: To study the effects of annexins II and V on the survival and neurite outgrowth of primary cultured neuronsand the survival of astrocytes after peroxide and hypoxia insults in vitro. METHODS: Annexins II and V proteinsand/or corresponding antibodies were added to the medium of primary neocortical cultures. H2O2 and NaN3 wereused to induce neuron injury, respectively. Lactate dehydrogenase (LDH) release was measured. RESULTS:Addition of annexin II or V into the culture medium did not affect the normal survival and neurite outgrowth ofcortical neurons. However, when an antibody against annexin II or V was added to the culture, the survival andneurite outgrowth of these neurons markedly declined. Further, addition of the two annexins into cortical culturesafter peroxide and hypoxia insults markedly reduced the LDH release and cell death. CONCLUSION: Annexins IIand V are essential for the survival and neurite outgrowth of developing cortical neurons, the survival of glial cells,and protect neurons and glial cells against peroxide and hypoxia injuries.

关键词： annexin II annexin V neurons astrocytes cell culture lactate dehydrogenases hydrogen peroxide hypoxia

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RNase MRP RNA and human genetic diseases

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Cell Research 2007年第3期17卷 219-226页

作者： Allison N Martin department of Biochemistry and Molecular Biology and Center for Genetics and Molecular medicine school of medicine university of louisville 319 Abraham Flexner Way KY 40202 usa

RNase MRP RNA is the RNA subunit of the RNase mitochondrial RNA processing(MRP)enzyme complex that isinvolved in multiple cellular RNA processing *** on RNase MRP RNA gene(RMRP)cause a recessivelyinherited developmental disorder,cartilage-hair hypoplasia(CHH).The relationship of the genotype(RMRP mutation),RNA processing deficiency of the RNase MRP complex,and the phenotype of CHH and other skeletal dysplasias is yetto be explored.

关键词： RNase MRP RNA cartilage-hair hypoplasia

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Rho与中枢神经系统轴突再生

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生物化学与生物物理进展 2004年第4期31卷 296-298页

作者：于盼盼徐晓明陆佩华上海第二医科大学神经生物学实验室上海200025

Rho是小分子质量GTP酶Rho家族成员 ,在细胞的一些信号转导途径中起着分子开关的作用 .Rho能通过作用于肌动蛋白骨架系统引起轴突生长锥塌陷 ,从而抑制轴突生长 .研究表明 ,Nogo A、MAG、OMgp等髓鞘源性的轴突再生抑制分子均可通过激活Rh... 详细信息

Rho是小分子质量GTP酶Rho家族成员 ,在细胞的一些信号转导途径中起着分子开关的作用 .Rho能通过作用于肌动蛋白骨架系统引起轴突生长锥塌陷 ,从而抑制轴突生长 .研究表明 ,Nogo A、MAG、OMgp等髓鞘源性的轴突再生抑制分子均可通过激活Rho介导的信号转导途径抑制轴突再生 .

关键词： Rho GTP酶中枢神经系统轴突再生信号转导

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Consensus of Chinese experts on glioma multidisciplinary team management(2nd edition)

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Chinese Medical Journal 2024年第11期137卷 1267-1270页

作者： Jinsong Wu Zhirui Zhou Zanyi Wu Zhiwei Tang Ming Li Siyuan Yin Xufei Luo Ling Wang Yaolong Chen Guoguang Zhao Tao Jiang Ying Mao The National Glioma MDT Alliance of National Center for neurological Diseases department of Neurosurgery Huashan HospitalShanghai Medical CollegeFudan UniversityShanghai 200040China department of Radiation Oncology Huashan HospitalShanghai Medical CollegeFudan UniversityShanghai 200040China department of Neurosurgery The First Affiliated Hospital of Fujian Medical UniversityFuzhouFujian 350005China Neurosurgery department The First Affiliated Hospital of Kunming Medical UniversityKunmingYunnan 650032China department of Neurosurgery Henan Provincial People’s HospitalPeople’s Hospital of Zhengzhou UniversityZhengzhouHenan 463599China State Key Laboratory of Pharmaceutical Biotechnology Institute for Brain SciencesAdvanced Institute for Life SciencesSchool of Life SciencesNanjing UniversityNanjingJiangsu 210023China Evidence-Based medicine Center School of Basic Medical SciencesLanzhou UniversityLanzhouGansu 730000China school of Public Health Lanzhou UniversityLanzhouGansu 730000China department of Neurosurgery Xuanwu HospitalCapital Medical UniversityBeijing 100053China department of Neurosurgery Beijing Tiantan HospitalCapital Medical UniversityBeijing 100050China 不详

To increase the consistency of glioma multidisciplinary team(MDT)management across different regions and hospitals at varying levels,we have updated the Expert Consensus on MDT of Glioma in China based on the currently available *** version has revised and updated the process-management rules and quality-control standards for a glioma MDT,providing reference and guidance for relevant clinical disciplines and *** members of the Consensus Expert Group,abstract,background,and prospects can be seen in supplementaryle,http://***/CM9/B999.

关键词： glioma MDT Expert

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Neuroprotective effect of ONO-1078, a leukotriene receptor antagonist, on transient global cerebral ischemia in rats

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Acta Pharmacologica Sinica 2003年第12期24卷 67-73页

作者： ZHANG Li-Hui~(2,3), WEI Er-Qing~(2,4) ~2department of Pharmacology, school of medicine, Zhejiang university, Hangzhou 310031 ~3Medical school, Hangzhou Teachers College, Hangzhou 310012, China department of Pharmacology School of Medicine Zhejiang University Hangzhou 310031

AIM: To determine whether ONO-1078 {pranlukast, 4-oxo-8-[p-(4-phenylbutyloxy)benzoyl-amono]-2-(tetrazol-5-yl)-4H-1-benzopyran hemihydrate}, a potent leukotriene receptor antagonist, possesses a neuroprotective effect on global cerebral ischemia in rats, and to explore its possible mechanism of action. METHODS: Transient global cerebral ischemia was induced by four-vessel occlusion for 10 min and followed by 72-h reperfusion. ONO-1078 (0.03-0.3 mg/kg) and edaravone (MCI-186, 3-methyl-1-phenyl-2-pyrazolin-5-one, a neuroprotective agent) 10 mg/kg were ip injected 30 min before ischemia and 1 h after reperfusion, and once a day afterward. neurological outcome was evaluated before ischemia and 24, 48, 72 h after reperfusion. Neuron density, the expressions of N-methyl-Daspartate (NMDA) receptor subunit proteins (NR1, NR2A, NA2B) and vascular cell adhesion molecule 1(VCAM-1) in the cerebral cortex and hippocampus were measured at 72 h after reperfusion. RESULTS: ONO-1078 (0.1, 0.3 mg/kg) and edaravone (10 mg/

关键词： ONO-1078 brain ischemia leukotriene antagonists neuroprotective agents N-methyl-D-aspartate receptors vascular cell adhesion molecule-1

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Combination treatment of EGb761 and methylprednisolone reduces tissue damage and improves functional recovery after spinal cord injury in adult rats

Combination treatment of EGb761 and methylprednisolone reduc...

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中国神经科学学会第四次会员代表大会暨第七届全国学术会议

作者： Jian ZOU~1,Xiao-Yan JIANG~1,Pan-Pan YU~1,Liang XU~1,Zhi-Fang CHEN~1,Pei-Hua LU~(1*) Xiao-Ming XU~(1,2*) 1 department of Neurobiology,Shanghai Jiao Tong university school of medicine,Shanghai 200025,China:2 kentucky Spinal Cord Injury Research Center,department of neurological surgery,university of louisville school of medicine,louisville,usa

＜正＞Methylprednisolone（MP） has been widely used as a standard therapeutic agent for the treatment of spinal cord injury（SCI）.However,its beneficial effects are ***,the combination of MP and other pharmacological agents aimed at enhancing functional recovery is ***761,a standardized Ginkgo Biloba extract（EGb）,has been implicated in neuroprotection through its antioxidation and anti-inflammatory *** the present study,we sought to determine the effects of MP and EGb761,administered individually or in combination,after a T9 contusive SCI in adult rats. Compared with the use of EGb761 or MP alone,the combination treatment significantly accelerated the recovery of locomotor and sensory functions compared to the MP or EGb761 ***,the combined treatment promoted motoneuron survival,reduced demyelination,and decreased the size of cavities at and surrounding the injury ***,the combination treatment reduced the expression of ED-1 and glial fibrillary acidic protein（GFAP） following ***,our study strongly suggested that the combination treatment with MP and EGb761 may represent a promising strategy to reduce injury-induced tissue damage and improve motor and sensory functions following SCI.

关键词： spinal cord injury EGb761 methylprednisolone locomotor neuron myelin astrocyte

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Development of novel therapies for Huntington's disease:hope and challenge

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Acta Pharmacologica Sinica 2005年第2期26卷 129-142页

作者： Zheng-hong QIN~(2,3,5),Jin WANG~4,Zhen-lun GU~2~2department of Pharmacology,Soochow university school of medicine,Suzhou 215007,China ~3Laboratory of Cellular Neurobiology,Massachusetts General Hospital and Harvard Medical school,Charlestown,MA 02129,usa ~4Molecular Neurogenetics Unit,Center forHuman Genetics Research,Massachusetts General Hospital and Harvard Medical school,Charlestown,MA 02129,usa department of Pharmacology Soochow University School of Medicine Suzhou China Laboratory of Cellular Neurobiology Massachusetts General Hospital and Harvard Medical School Charlestown USA Molecular Neurogenetics Unit Center for Human Genetics Research Massachusetts General Hospital and Harvard Medical School Charlestown USA

Huntington's disease(HD)is an autosomal dominant neurological *** is afatal neurological disorder affecting 5-10 out of 10000 *** there areintensive research efforts focusing on uncovering molecular mechanisms of thepathogenesis of HD,a number of studies have begun to look for effective thera-pies for *** is a large body of encouraging news on novel *** present paper reviews drugs used for symptomatic treatmentof HD and experimental therapies targeting HD molecular pathology.

关键词： Huntington disease huntingtin aggregates caspases nerve growth factors cell transplantation coenzyme Q10

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