title: Alteration in the differentiation-related molecular expression in the subventricular zone in a mouse model of Parkinson's disease.
abstract: Enhancement of neurogenesis could be a suitable treatment approach to up-regulate dopaminergic neurons in Parkinson's disease (PD). In the present study, we focused on the kinetics of the subventricular zone (SVZ) in a mouse model of PD induced by MPTP injection. We showed recently the proliferation potential of neuronal stem cells (NSCs) prepared from the olfactory bulb of an animal model of PD [Hayakawa, H., Hayashita-Kinoh, H., Nihira, T., Seki, T., Mizuno, Y., Mochizuki, H., 2007. The isolation of neural stem cells from the OB of Parkinson's disease model. Neurosci. Res.]. In this study, we examined the relationship between proliferation and differentiation of NSCs in SVZ of both acute and chronic PD models. Only acute MPTP treatment significantly increased the areas of glial fibrillary acidic protein (GFAP)-expressing cells and decreased the areas of polysialylated neural cell adhesion molecule (PSA-NCAM)-expressing cells in the SVZ. In the case of caspase-11 knockout mice, MPTP did not induce alteration in the areas of GFAP-expressing cells and PSA-NCAM-expressing cells. Our results suggest that neuroinflammation related to the caspase-11 cascade in the striatum regulates differentiation of neural stem cells in the SVZ of our mouse model of PD.
authors.affiliation: Department of Neurology, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo, Tokyo 113-8421, Japan.
authors.forename: Hideki
authors.initials: H
authors.lastname: Oizumi
authors.forename: Hiromi
authors.initials: H
authors.lastname: Hayashita-Kinoh
authors.forename: Hideki
authors.initials: H
authors.lastname: Hayakawa
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Arai
authors.forename: Tsuyoshi
authors.initials: T
authors.lastname: Furuya
authors.forename: Yong-Ri
authors.initials: YR
authors.lastname: Ren
authors.forename: Toru
authors.initials: T
authors.lastname: Yasuda
authors.forename: Tatsunori
authors.initials: T
authors.lastname: Seki
authors.forename: Yoshikuni
authors.initials: Y
authors.lastname: Mizuno
authors.forename: Hideki
authors.initials: H
authors.lastname: Mochizuki
mesh_terms: D015632:1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine; D000208:Acute Disease; D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D020169:Caspases / Q000235:genetics / Q000378:metabolism*; D053471:Caspases, Initiator; D002452:Cell Count; D016923:Cell Death / Q000187:drug effects / Q000502:physiology; D002454:Cell Differentiation / Q000187:drug effects / Q000502:physiology*; D002465:Cell Movement / Q000502:physiology; D049109:Cell Proliferation / Q000187:drug effects; D002908:Chronic Disease; D004195:Disease Models, Animal; D004660:Encephalitis / Q000378:metabolism* / Q000503:physiopathology; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D020547:Lateral Ventricles; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009416:Nerve Regeneration / Q000187:drug effects / Q000502:physiology; D039842:Neural Cell Adhesion Molecule L1 / Q000378:metabolism; D009498:Neurotoxins; D020734:Parkinsonian Disorders / Q000378:metabolism* / Q000503:physiopathology; D020127:Recovery of Function / Q000187:drug effects / Q000502:physiology; D012794:Sialic Acids / Q000378:metabolism; D013234:Stem Cells / Q000166:cytology / Q000378:metabolism*; D013687:Telencephalon / Q000378:metabolism* / Q000503:physiopathology
chemical_list: D015415:Biomarkers; D005904:Glial Fibrillary Acidic Protein; D039842:Neural Cell Adhesion Molecule L1; D009498:Neurotoxins; D012794:Sialic Acids; C103469:polysialyl neural cell adhesion molecule; D015632:1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine; C101136:Casp4 protein, mouse; D020169:Caspases; D053471:Caspases, Initiator