Capucin does not modify the toxicity of a mutant Huntingtin fragment in vivo

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• 作者：Laurie Galvan^a ; ^b ; Nad'a Lepejová ; ^c ; Marie-Claude Gaillard^a ; ^b ; Carole Malgorn^a ; ^b ; Martine Guillermier^a ; ^b ; Diane Houitte^a ; ^b ; Gilles Bonvento^a ; ^b ; Fanny Petit^a ; ^b ; No&euml ; lle Dufour^a ; ^b ; Patrick Hé ; ry^c ; Matthieu Gé ; rard^c ; Jean-Marc Elalouf^c ; Nicole Dé ; glon^a ; ^b ; Emmanuel Brouillet^a ; ^b ; ¹ ; ^{emmanuel.brouillet@cea.fr} ; Michel de Chaldé ; e^c ; ¹ ; ^{michel.de.chaldee@cea.fr}
• 关键词：Huntington's disease ; Capucin ; Neurodegeneration ; Basal ganglia ; Striatal marker ; Lentiviral vectors ; Knockout mice
• 刊名：Neurobiology of Aging
• 出版年：2012
• 期刊代码：202_01974580
• 类别：med
• 出版时间：August, 2012
• 卷：33
• 期：8
• 页码：1845.e5-1845.e6
• 文件大小：329 K

摘要

Genes selectively expressed in the striatum may be involved in the preferential vulnerability of striatal neurons to Huntington's disease (HD). Here, we investigated whether perturbations of Capucin expression, which is enriched in the striatum and downregulated in Huntington's disease models, could modify the neurotoxicity induced by the injection of a lentiviral vector encoding a short N-terminal fragment of mutant Huntingtin (mHtt) into the mouse striatum. Neither constitutive Capucin deficiency in knockout mice nor lentiviral vector-mediated Capucin overexpression in the striatum of adult wild type mice significantly modified vulnerability to the mHtt fragment in vivo, suggesting that Capucin has no impact on mHtt toxicity.