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intercellular adhesion molecule-5 protects PAJU cells during in vitro ischemia following cerebral infarction

Neural Regeneration Research 2010年第3期5卷 205-208页

作者： Weijun Zhou Heping Yang Xiang Wang Yi Peng Dapeng WU Xiaojie Zhang Zhiping Hu Department of Neurology Second Xiangya Hospital Central South University Changsha 410011 Hunan Province China Department of Neurology Ruikang Hospital Affiliated to Guangxi Traditional Chinese Medical University Nanning 530011 Guangxi Zhuang Autonomous Region China Department of Psychiatry Second Xiangya Hospital Central South University Changsha 410011 Hunan Province China

BACKGROUND： intercellular adhesion molecule-5 （ICAM-5） relieves the damage of beta-amyloid protein to PAJU cells, However, little is known about how ICAM-5 works as a neurotrophic factor, or whether ICAM-5 lessens neuronal damage under ischemic conditions following cerebral infarction. OBJECTIVE： To investigate the effects of ICAM-5 on PAJU cells growth in serum-free medium under ischemic conditions following cerebral infarction. DESIGN, TIME AND SETTING： The cytological in vitro study was performed at the Central Laboratory, Second Xiangya Hospital, Central South University, China, in June 2009. MATERIALS： Human ICAM-5 gene transfected into PAJU-TLN cells was supplied by the Life Science College, Helsinki University, Finland. Empty vector transfected PAJU-NEO cells were established by the Gene Center, Second Xiangya Hospital, Central South University, China. METHODS： PAJU-TLN cells transfected with human ICAM-5 or empty vector were incubated in serum-free medium. MAIN OUTCOME MEASURES： Phase contrast microscopy was used to observe changes in PAJU cell morphology. 3-（4, 5-dimethylthiazolzyl）-2, 5-diphenyltetrazolium bromide was used to determine cell viability. Hoechst 33258 was used to stain cell nuclei. Flow cytometry was utilized to measure the apoptosis rate of both PAJU-TLN and PAJU-NEO cells. RESULTS： Both PAJU-TLN and PAJU-NEO cells were injured by cultivating in serum-free medium, but the survival rate of PAJU-TLN cells was significantly higher. CONCLUSION： ICAM-5 protects PAJU-TLN cells from serum deprivation-induced apoptosis, induces the outgrowth of PAJU cells, and diminishes their morphologic impairment.

关键词： intercellular adhesion molecule-5 cerebral infarction serum deprivation neuroprotective effect brain injury

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Calsyntenin-1 Implicates in Dendritic Spine Abnormalities in Fragile X Syndrome Mouse Model by Modulating Dendritic ICAM5 Redistribution

Calsyntenin-1 Implicates in Dendritic Spine Abnormalities in...

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中国神经科学学会第十二届全国学术会议

作者： Ke Cheng Yan Zeng Qiong Zhu Zhi-wei Zhang Gui-rong Cheng Dan Liu Brain and Cognitive Function Laboratory Wuhan University of Science and Technology

Objective Our prior studies have demonstrated the critical role of the neuronspecific intercellular adhesion molecule 5（ICAM5, telencephalin） in spine development and revealed its implication in the dendritic spine maturation of fragile X syndrome（FXS）. But, the molecular mechanism that results in ICAM5 dysregulation in FXS has not been studied yet. The present study is to explore the role of calsyntenin-1（Clstn1）, type-1 transmembrane proteins of the cadherin superfamily, in spine maturation in FXS neurons, and whether it mediates intracellular transportation of ICAM5 and redistribution. Methods Fmr1 knock out（KO）（FVB 129 P2-Pde6 b+ Tyrc-ch-Fmr1 tm1 Cgr/J） and control（FVB.129 P2-Pde6 b Tyrc-ch/Ant J）, here-after referred to as wild-type（WT） strain mice were used as the animal model of FXS. Primary mouse neuronal cultures were generated from prefrontal cerebral cortex of WT or Fmr1-KO embryos（E17–E18）. The interaction between Clstn1 and Icam5 was identified by live cell imaging and time-lapse analysis, immunocytochemistry and colocalization. The alteration of dendritic spine in neurons was measured by confocal analysis. The pattern of postnatal spine development was profiled by Golgi staining. Results（1） Fmr1 KO presented anomalous postnatal dendritic spines that are concomitant to abundant ICAM5 expression and decreased synaptic calsyntenin-1 in a few brain areas.（2） Clstn1 was colocalized with Icam5 in cultured mouse neurons and in N2 a cell line.（3） Clstn1 deletion in neurons resulted in increased expression of Icam5 on membrane and redistribution in neurons, while reexpression of Clstn1 normalized Icam5 distribution.（4） Clstn1 deletion in neurons resulted in decreased dendritic arborization and increased proportions of immature filopodia-like dendritic protrusions, while re-expression of Clstn1 rescued the spine retraction response. Conclusion Clstn1 mediates ICAM5 redistribution, and further promotes spine maturation. In its dysregulation in Fmr1 KO mice, the f

关键词： Calsyntenin-1 intercellular adhesion molecule-5 dendritic spine intracellular transport Fragile X syndrome

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The FMRP/ICAM5 mRNA Interaction Uncovers a New Mechanism of Modulating Dendritic Spine Development and Cognitive Behaviors in Fragile X Syndrome

The FMRP/ICAM5 mRNA Interaction Uncovers a New Mechanism of ...

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中国神经科学学会第十二届全国学术会议

作者： Ya-Ping Pei Yan Zeng Shi-jing Yuan Mi Tian Lang Xu Qiong Zhu Ming-Gao Zhao Brain and Cognitive Function Laboratory Wuhan University of Science and Technology

Objective Fragile X syndrome（FXS） is the most common cause of intellectual disability in males and the most common single gene cause of autism. Dendrite and spine abnormalities have been correlated with impaired cognitive abilities in FXS, where neurons show a high density of long, thin, and immature dendritic spines. But the causes of these malformations are not yet well understood. intercellular adhesion molecule 5（ICAM5;Telencephalin）, a protein of the Ig superfamily, has been implicated in neuronal and spine development as well as the formation and maintenance of dendritic filopodia. The present study is to examine a possible link for ICAM5 in Fmr1 knockout（KO） mice, the animal model of FXS and to futher investigate the direct interaction of FMRP and ICAM5. Methods Fmr1 knock out（KO）（FVB 129 P2-Pde6 b+Tyrc-ch-Fmr1 tm1 Cgr/J） and control（FVB.129 P2-Pde6 b Tyrc-ch/Ant J）, here-after referred to as wild-type（WT） strain mice were used as the animal model of FXS. Primary mouse neuronal cultures were generated from prefrontal cerebral cortex of WT or Fmr1-KO embryos（E17–E18）. The pattern of postnatal spine development and ICAM5 expression was profiled by Golgi staining and western blot respectively. The interaction between Clstn1 and Icam5 m RNA was identified by RNA binding protein immunoprecipitation and quantitative real-time PCR. The alteration of dendritic spine in neurons was measured by live cell imaging. Results（1） In Fmr1 KO brains and cultured neurons, ICAM5 m RNA translation was enhanced by the loss of FMRP, leading to excessive production of ICAM5 protein and preventing filopodiato-spine transition, but ICAM5 m RNA was less affected.（2） Genetic reduction of ICAM5 by using si RNA ICAM5 normalized the aberrant spine maturation and ameliorated behavior impairments including spatial and fear memory in Fmr1 KO mice.（3） FMRP was immunoprecipitated with ICAM5 m RNA from mouse brain and the binding region in ICAM5 was localized to the two first Ig domains. Conclus

关键词： Fragile X syndrome fragile X mental retardation protein intercellular adhesion molecule-5 dendritic spine interaction

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