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Endothelial cell migration-associated vessel pruning is essential for brain vascular development in vivo

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Endothelial cell migration-associated vessel pruning is esse...

2010·第一届斑马鱼学术研讨会

作者： Qi Chen,Luan Jiang,Chun Li,Jiwen Bu,Jiulin Du~* institute of neuroscience and state key laboratory of neuroscience,shanghai institutes for biological sciences,chinese academy of sciences,320 Yue-Yang Road,shanghai 200031, china

During vascular development,it is believed that the primitive vascular plexus is extensively remodeled via sprouting new blood vessels and pruning of existing *** evidence for vascular pruning has been shown in the hy...

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*** as a model system for Parkinson disease

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neuroscience Bulletin 2006年第2期22卷 124-128页

作者： Pu PU,Wei-Dong le state key laboratory of Medical Genomics,Ruijin Hospital,shanghai Jiao Tong University School of Medicine institute of Health sciences,shanghai institutes for biological sciences,chinese academy of sciences-shanghai Jiao Tong University School of Medicine,shanghai 200031,china statekeylaboratoryofMedicalGenomics RuijinHospitalShanghaiJiaoTongUniversitySchoolofMedicine instituteofHealthsciences ShanghaiInstitutesforBiologicalSciencesChineseAcademyofSciences-ShanghaiJiaoTongUniversity

Parkinson disease(PD) is characterized by the selective loss of dopaminergic neurons in the substantia nigra. Although investigation in mammalian animal models of PD has enhanced our understanding of PD, the complexity of the mammalian nervous system and our inability to visualize DA neurons in vivo restricts the advances in elucidating the molecular mechanisms of PD. Conservation between C. elegans and mammals in genomic, biosynthetic and metabolic pathways as well as the advantages of observing DA neurons morphology in vivo and the ease of transgenic and genetic manipulation make C. elegans an excellent model organism for PD.

关键词： caenorhabditis elegans( C. elegans) Parkinson disease dopaminergic neuron

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FGF13A represses transcription of rRNA genes as a nucleolar protein

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FGF13A represses transcription of rRNA genes as a nucleolar ...

中国神经科学学会第四次会员代表大会暨第八届全国学术会议

作者： Liu YANG~1,Lan BAO~2,xu ZHANG~(1,*) 1 institute of neuroscience and state key laboratory of neuroscience 2 institute of Biochemistry and Cell Biology and laboratory of Molecular Cell Biology,shanghai institutes for biological sciences,chinese academy of sciences,shanghai,200031,china

Objective Fibroblast growth factors(FGFs) are among the first-indentified families of growth *** are polypeptides with diverse biological activities including cell proliferation,differentiation,migration and so *** their functions are much more evident in the nervous system than in *** FGFs have N-terminal signal peptides and can be secreted ***,FGF11 subfamily(FGFs 11-14) is a special *** FGFs lack signal peptides, remain intracellularly and function within cells in a receptor-independent manner,hereafter referred to as *** growth factor 13(FGF13) is a member of the intracellular FGF homologous factor subfamily(iFGFs) and highly expressed in nervous system,however its functions are still *** The subcellular localization of FGF13A was investigated by *** interaction between FGF13A and UBF1 was investigated by coimmunoprecipitation (co-IP) *** function of FGF13A on the neurite outgrowth of DRG neurons was investigated by electroporation and ***(1) The expression of FGF13A-EGFP in transfected ND7-23 cells or dissociated primary DRG neurons was highly enriched in the nucleolus of the two types of cells and colocalized with the nucleolus marker,fibrillarin and nucleolin.(2) Overexpression of FGF13A repressed rRNA transcription through interacting with upstream binding factor 1(UBF1),a RNA pol I transcription factor.(3) Overexpression of FGF13A significantly inhibited neurite outgrowm of dissociated DRG *** Nucleolus-localized FGF13A represses rRNA transcription and therefore inhibits DRG neurite outgrowth.

关键词： iFGF UBF1 ribosomal RNA transcription neurite outgrowth

A Cl--regulated structural switch that controls proton sensitivity of acid-sensing ion channels

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A Cl--regulated structural switch that controls proton sensi...

中国神经科学学会第九届全国学术会议暨第五次会员代表大会

作者： Wei-Guang LI~(1,2),Zhu-Dan ZHANG~(1,2),Hui CAO~1,tian-le xu~(1,3,*) 1 institute of neuroscience and state key laboratory of neuroscience,shanghai institutes for biological sciences, chinese academy of sciences,shanghai 200031 2 Graduate School of chinese academy of sciences,shanghai 200031,china 3 institute of Medical sciences,shanghai Jiaotong University,shanghai 200025

Acid-sensing ion channel(ASIC) has a prominent role in tissue pH-sensing and neuronal signaling,and participates in various pathological *** the availability of structures for chicken ASIC1 subunit, obtaining mechanistic insight into the function of these highly dynamic channel proteins using static crystallographic information is *** a series of mutational,chemical and functional approaches,we found that the extracellular CI-binding module shown in crystals of ASIC1 constitutes an indispensable component for ASIC1a *** gluconate-substitution of natural CI-binding enhanced whereas engineering a permanent anion into the CI-binding module inhibited channel activity,suggesting an essential role of CI-regulated domain flexibility but not the absolute charge state created by bound anion in channel ***-comparable anion substitution(F, Br-,or I) revealed a CI-dependent modulation of proton sensing function,supporting a structural role of dynamic association and dissociation of CI ion in coordinating conformational transition associated with proton sensing. Furthermore,charge reversal and swap as well as mutant cycle analysis of alanine substitutions of two counter-charged residues(K311,E315) in the CI-binding module show that they electrostatically interacted and energetically coupled, underpinning a structural switch controlling proton sensitivity of ASIC1a channels.

关键词： acid-sensing ion channel channel gating salt bridge

Apoptosis initiated by carbon tetrachloride in mitochondria of rat primary cultured hepatocytes

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Acta Pharmacologica Sinica 2005年第8期26卷 969-975页

作者： Yan CAI~(1,2), Li-kun GONG~(1,2), Xin-ming QI~(1,2), xiang-hong LI~1, Jin REN~(1,3) ~1state key laboratory of Drug Researeh, shanghai institute of Materia Medica, shanghai institutes for biological sciences, chinese academy of sciences, shanghai 201203, china ~2Graduate School of the chinese academy of sciences, shanghai 201203, china state key laboratory of Drug Research Shanghai Institute of Materia Medica Shanghai Institutes for Biological Sciences Chinese Academy of Sciences Shanghai 201203 China

Aim: To investigate the mitochondria-initiated apoptosis pathway involved in Carbon tetrachloride （CCl4） hepatotoxicity in vitro. Methods: Several cytotoxic-ity endpoints, including WST-8 metabolism, lactate dehydrogenase leakage and morphological changes, were examined. The 5,5'-dithio-bis（2-nitrobenzoic acid） reaction was used to measure reduced glutathione level, and the malondialdehyde level was determined using the thiobarbituric acid assay. The release of cyto-chrome c and Bcl-XLwas detected by Western blot. Caspase-3 activity was mea sured using the fluorogenic substrate Ac-DEVD-AMC. DNA fragmentation wasused to evaluate cell apoptosis. Results: A time-and dose-dependent decrease in cellular glutathione content was observed, along with a concomitant increase in malondialdehyde levels following the application of CCl4. Caspase 3 activity was stimulated at all doses of CCl4, with the most significant activation at 3 mmol/L. Cytochrome c was released obviously after CCl4treatment. A time-dependent decrease in BcI-Xlexpression was observed. DNA fragmentation results revealed apoptosis and necrosis following CCl4treatment. Conclusion: Oxidative damage is one of the essential mechanisms of CCl4hepatotoxicity, which triggers apoptosis via the mitochondria-initiated pathway.

关键词： carbon tetrachloride hepatocytes mitochondria caspase 3 cytochrome c

Early lung injury contributes to lung fibrosis via AT1 receptor in rats

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Acta Pharmacologica Sinica 2007年第2期28卷 227-237页

作者： Fang-ping CHEN~(1,2) Li-kun GONG~1 Ling ZHANG~3 Hui wang~(1,2) Xin-ming QI~(1,2) Xiong-fei WU~(1,2) Ying XIAO~(1,2) Yan CAI~(1,2) Lin-lin LIU~(1,2) xiang-hong LI~1 Jin REN~(1,4)1 state key laboratory of Drug Research,shanghai institute of Materia Medica,shanghai institutes for biological sciences,chinese academy of sciences,shanghai 201203,china 2 Graduate School of the chinese academy of sciences,shanghai Branch,shanghai 200031,china 3 shanghai Pulmonary Hospital,shanghai 200043,china state key laboratory of Drug Research Shanghai Institute of Materia MedicaShanghai Institutes for Biological SciencesChinese Academy of SciencesShanghai 201203China Graduate School of the chinese academy of sciences Shanghai BranchShanghai 20003 shanghai Pulmonary Hospital Shanghai 200043China

Aim:Angiotensin Ⅱ is believed to play an important role in tissue repair andremodeling in lungs by the angiotensin type I(AT1)receptor via a number ofpotential ***,the role of the AT1 receptor in early lung injuryhas not been ***:Bleomycin-induced pulmonary fibrosis(PF)in rats was utilized to value the treatment with valsartan,an AT1 receptorantagonist,by measurement of body weight,wet weight of the left lung,hydroxy-proline content,mRNA expression of collagen Ⅰ/Ⅲ,and the degree of fibrosis inlung tissues on d *** injury in the early phase was assessed on d 1,3 and7 by apoptosis,malondialdehyde content,myeloperoxidase activity,inflamma-tory cell count and protein *** converting enzyme(ACE)activ-ity and the AT1 receptor in lung tissues were analyzed by biochemistry methodand Western blotting,***:Valsartan ameliorated PF induced bybleomycin in the rats on d *** bleomycin was injected intratracheally,in-creases in the lung AT1 receptor and ACE activity were observed by d 1,3 and *** injury deteriorated in the early *** reduced the increase of theAT1 receptor,ACE activity and lung injury induced by bleomycin in the ***:These observations suggest that angiotensin Ⅱ may play apotent role in early lung injury via the AT1 ***1 receptor antagonistsshould be assessed as potential new therapies for fibrotic lung disease.

关键词： angiotensin II AT1 receptor pulmonary fibrosis lung injury

Fibroblast growth factor 7 acts as a modulator of nociception

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Fibroblast growth factor 7 acts as a modulator of nociceptio...

中国神经科学学会第九届全国学术会议暨第五次会员代表大会

作者： Hui LIU~1,Qing-Feng WU~1,Qiong wang~2,Lan BAO~2,xu ZHANG~1 1 institute of neuroscience and state key laboratory of neuroscience,2 institute of Biochemistry and Cell Biology and laboratory of Molecular Cell Biology,shanghai institutes for biological sciences,chinese academy of sciences, shanghai 200031,china

＜正＞Fibroblast growth factor（FGF）7,which is also known as keratinocyte growth factor（KGF）,is a member of the FGF *** studies regard it as a locally acting epithelial mitogen that is produced by cells of mesenchymal origin and has an important role in protecting and repairing epithelial ***,its potential functions in the nervous system are poorly *** found that FGF7,together with its high-affinity receptor FGFR2b,was expressed in both dorsal root ganglion（DRG）and spinal cord ***7 mRNA was consistently increased in DRGs after peripheral nerve injury and transiently up-regulated after intraplantar injection of complete Freund’s *** injection of recombinant human FGF7 exacerbated the formalin-induced hyperalgesia, while application with either the antibodies against FGF7 or recombinant FGF R2β（Ⅲb）Fc chimera alleviated inflammatory nociceptive ***,behavior tests and wide-dynamic range neuron recordings of FGF7 knockout mice showed a defect in nociceptive *** together,these results suggest that FGF7 may contribute to inflammatory pain sensation and play an important role in nociceptive transmission.

关键词： fibroblast growth factor 7 inflammatory pain nociceptive transmission

Isolation and functional characterization of the C-terminus of rice phos-phatidylinositol 4-kinase in vitro

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Cell Research 2003年第2期13卷 131-139页

作者： xiang FENG KONG, ZHI HONG xu, HONG WEI xuE, National laboratory of Plant Molecular Genetics, institute of Plant Physiology and Ecology, shanghai institutes for biological Science (SIBS), The chinese academy of sciences Partner Group of Max-Planck-institute of Molecular Plant Physiology (MPI-MP) on "Plant Molecular Physiology and Signal Transduction", 300 Fenglin Road, 200032 shanghai, china 1National laboratory of Plant Molecular Genetics Institute of Plant Physiology and Ecology Shanghai Institutes for Biological Science (SIBS)The Chinese Academy of Sciences Partner Group el Max-Planck-institute of Molecular Plant Physiology (MPI-MP) on “Plant Molecular Physiology and Signal Transduction” 300 Fenglin Road 200032 Shanghai China 1National laboratory of Plant Molecular Genetics Institute of Plant Physiology and Ecology Shanghai Institutes for Biological Science (SIBS)The Chinese Academy of Sciences Partner Group el Max-Planck-institute of Molecular Plant Physiology (MPI-MP) on “Plant Molecular Physiology and Signal Transduction” 300 Fenglin Road 200032 Shanghai China 1National laboratory of Plant Molecular Genetics Institute of Plant Physiology and Ecology Shanghai Institutes for Biological Science (SIBS)The Chinese Academy of Sciences Partner Group el Max-Planck-institute of Molecular Plant Physiology (MPI-MP) on “Plant Molecular Physiology and Signal Transduction” 300 Fenglin Road 200032 Shanghai China

A partial rice (Oryza sativa L.) cDNA clone. OsPMK1c, was isolated through screening of a cDNA library constructed from tillering materials. OsPI4Klc encoded a peptide of 608 amino acids with a calculated molecular mass of 68.4 kDa. The OsPI4Klc peptide shared high homology and possessed the highly conserved domains present in most isolated cloned PI4-kinases, i.e. a lipid kinase unique (LKU) domain and a catalytic (CAT) domain. A region with similarity to pleckstrin homology (PH) domain was present in OsPI4K1c as well. Further comparison with genomic sequences in databases revealed that OsPI4K1c is located at the 3'-end of a putative rice PI 4-kinase coding gene OsPI4K1, and its coding region corresponded to the C-terminal half of OsPI4Kl protein. Twelve exons (49-562 bp in size) and 11 introns (77-974 bp in size) were identified in OsPI4K1c. The recombinant protein expressed in Escherichia coli phosphorylates phosphatidylinositol at the D4 position of the inositol ring. OsPI4K1 transcript levels were

关键词： Oryza sativa phosphatidylinositol 4-kinase.

Tri-lithium pyrroloquinoline quinine ameliorates cognitive impairment and extenuates cerebral pathological lesions in amyloid precursor protein/presenilin-1 transgenic mice

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Tri-lithium pyrroloquinoline quinine ameliorates cognitive i...

中国神经科学学会第九届全国学术会议暨第五次会员代表大会

作者： lei ZHAO~1,Neng GONG~2,Zhe YU~2,Qi FANG~2,tian-le xu~(2,*),Chun-Jiu ZHONG~(1,*) 1 Department of Neurology,Zhongshan Hospital,Fudan Univeristy,shanghai 200032,china 2 institute of neuroscience,state key laboratory of neuroscience,shanghai institutes for biological sciences,chinese academy of sciences,shanghai 200031,china

Alzheimer’s disease(AD) is the most common age-related neurodegenerative disorder and cause of dementia in the elderly,characterized by global cognitive impairment and the presence of extracellular beta-amyloid (Aβ) deposition(senile plaques) and intracellular hyperphosphorylated tau protein(neurofibrillary tangles).Currently, the dominant theory to explain pathogenesis of AD is the "Amyloid Cascade Hypothesis" first proposed in 1992. However,almost all previous clinical trials targeting Aβhave received negative *** disappointing fact triggers us to reconsider this hypothesis and to explore more effective treatment *** drastic disturbance of glucose metabolism in the brain is one of the striking features of AD.A significant reduction in cerebral glucose consumption precedes overt clinical symptoms or brain atrophy,even for *** studies have demonstrated multiple defects in glucose and energy metabolism in AD ***,the decreased glucose and energy metabolism induces various pathogeneses similar to AD such as oxidative stress,activated glucose synthase kinase-3(GSK-3) signal pathway,and excitatory and inhibitory signaling dysfunction,and so ***,the drug or therapy only targeting to a single mechanism is difficult to modify the *** is essential to design new treatment strategy that can rectify the disturbed cellular energy metabolism and stop the multiple pathogenic cascades ***,a GSK- 3 inhibitor,has been demonstrated the beneficial effect on *** quinone,a new B vitamin,has been demonstrated neuroprotective action through the mechanisms of powerful anti-oxidation and improving mitochondria *** independently synthesized tri-lithium pyrroloquinoline quinone(LiPQQ).We found that LiPQQ exhibited a very low acute toxicity(LiPQQ ID50 2.50 g/kg weight vs LiC1 ID50 0.53 g/kg weight) by evaluating acute toxicity with *** use the amyloid precursor protein/presenilin-1(APP/PSl)

关键词： lithium pyrroloquinoline quinine Alzheimer’s disease