title: Sema4D deficiency results in an increase in the number of oligodendrocytes in healthy and injured mouse brains.
abstract: Semaphorins, a family of secreted and membrane-bound proteins, are known to function as repulsive axon guidance molecules. Sema4D, a class 4 transmembrane-type semaphorin, is expressed by oligodendrocytes in the central nervous system, but its role is unknown. In this study, the effects of Sema4D deficiency on oligodendrocytes were studied in intact and ischemic brains of adult mice. As observed in previous studies, Sema4D marked by beta-galactosidase in Sema4D mutant mice was localized exclusively on myelin-associated glycoprotein (MAG)-positive oligodendrocytes but not on NG2-positive oligodendrocyte progenitor cells (OPCs). Although there was no difference in the number of the latter cells between Sema4D-deficient and wild-type mice, the number of MAG-positive cells was significantly increased in the cerebral cortex of both nonischemic and postischemic brains of Sema4D-deficient mice. Cell proliferation, observed by using bromodeoxyuridine incorporation, was evident in the MAG-positive cells that developed after cerebral ischemia. These data indicate that Sema4D is involved in oligodendrogenesis during development and during recovery from ischemic injury.
authors.affiliation: Division of Pathogenesis and Control of Oral Diseases, Graduate School of Dentistry, Osaka University, Osaka, Japan.
authors.forename: Yoshitaka
authors.initials: Y
authors.lastname: Taniguchi
authors.forename: Mayumi
authors.initials: M
authors.lastname: Amazaki
authors.forename: Tatsuo
authors.initials: T
authors.lastname: Furuyama
authors.forename: Wataru
authors.initials: W
authors.lastname: Yamaguchi
authors.forename: Mizue
authors.initials: M
authors.lastname: Takahara
authors.forename: Orie
authors.initials: O
authors.lastname: Saino
authors.forename: Takeshi
authors.initials: T
authors.lastname: Wada
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Niwa
authors.forename: Fumi
authors.initials: F
authors.lastname: Tashiro
authors.forename: Jun-Ichi
authors.initials: J
authors.lastname: Miyazaki
authors.forename: Mikihiko
authors.initials: M
authors.lastname: Kogo
authors.forename: Tomohiro
authors.initials: T
authors.lastname: Matsuyama
authors.forename: Shinobu
authors.initials: S
authors.lastname: Inagaki
mesh_terms: D000818:Animals; D002452:Cell Count; D002454:Cell Differentiation; D002455:Cell Division; D002540:Cerebral Cortex / Q000473:pathology*; D005260:Female; D020244:Infarction, Middle Cerebral Artery / Q000378:metabolism / Q000473:pathology*; D002546:Ischemic Attack, Transient / Q000378:metabolism / Q000473:pathology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008813:Mice, Inbred ICR; D018345:Mice, Knockout; D009186:Myelin Sheath / Q000378:metabolism; D009836:Oligodendroglia / Q000166:cytology* / Q000473:pathology; D015427:Reperfusion Injury / Q000473:pathology*; D039961:Semaphorins / Q000172:deficiency / Q000235:genetics / Q000502:physiology*
chemical_list: C103150:Sema4d protein, mouse; D039961:Semaphorins