title: Adult CST-null mice maintain an increased number of oligodendrocytes.
abstract: The galactolipids galactocerebroside and sulfatide have been implicated in oligodendrocyte (OL) development and myelin formation. Much of the early evidence for myelin galactolipid function has been derived from antibody and chemical perturbation of OLs in vitro. To determine the role of these lipids in vivo, we previously characterized mice lacking galactocerebroside and sulfatide and observed abundant, unstable myelin and an increased number of OLs. We have also reported that mice incapable of synthesizing sulfatide (CST-null) while maintaining normal levels of galactocerebroside generate relatively stable myelin with unstable paranodes. Additionally, Hirahara et al. (2004; Glia 45:269-277) reported that these CST-null mice also contain an increased number of OLs in the forebrain, medulla, and cerebellum at 7 days of age. Here, we further the findings of Hirahara et al. by demonstrating that the number of OLs in the CST-null mice is also increased in the spinal cord and that this elevated OL population is maintained through, at least, 7 months of age. Moreover, we show that the enhanced OL population is accompanied by increased proliferation and decreased apoptosis of oligodendrocytic-lineage cells. Finally, through ultrastructural analysis, we show that the CST-null OLs exhibit decreased morphological complexity, a feature that may result in decreased OL competition and increased OL survival.
authors.affiliation: Department of Anatomy and Neurobiology, Virginia Commonwealth University, Richmond, Virginia, USA.
authors.forename: S M
authors.initials: SM
authors.lastname: Shroff
authors.forename: A D
authors.initials: AD
authors.lastname: Pomicter
authors.forename: W N
authors.initials: WN
authors.lastname: Chow
authors.forename: M A
authors.initials: MA
authors.lastname: Fox
authors.forename: R J
authors.initials: RJ
authors.lastname: Colello
authors.forename: S C
authors.initials: SC
authors.lastname: Henderson
authors.forename: J L
authors.initials: JL
authors.lastname: Dupree
mesh_terms: D000375:Aging / Q000235:genetics / Q000378:metabolism; D000818:Animals; D017209:Apoptosis / Q000235:genetics; D002452:Cell Count; D002454:Cell Differentiation / Q000235:genetics; D019070:Cell Lineage / Q000235:genetics; D049109:Cell Proliferation; D002470:Cell Survival / Q000235:genetics; D004195:Disease Models, Animal; D005786:Gene Expression Regulation / Q000235:genetics; D020279:Hereditary Central Nervous System Demyelinating Diseases / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology; D051379:Mice; D018345:Mice, Knockout; D009186:Myelin Sheath / Q000378:metabolism*; D009413:Nerve Fibers, Myelinated / Q000378:metabolism* / Q000648:ultrastructure; D009836:Oligodendroglia / Q000378:metabolism* / Q000473:pathology; D013116:Spinal Cord / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D013234:Stem Cells / Q000378:metabolism / Q000473:pathology; D013433:Sulfoglycosphingolipids / Q000378:metabolism*; D015238:Sulfotransferases / Q000235:genetics*; D015854:Up-Regulation / Q000235:genetics
chemical_list: D013433:Sulfoglycosphingolipids; D015238:Sulfotransferases; C020556:galactosylceramide sulfotransferase