title: Loss of polysialic residues accelerates CNS neural precursor differentiation in pathological conditions.
abstract: Using the model of lysolecithin-induced demyelination of the corpus callosum in wild-type, NCAM-deficient, and endoneuraminidase-injected mice, we have analyzed the consequences of the loss of expression of NCAM or PSA residues on the migration and proliferation capacities of neural precursors of the subventricular zone (SVZ). We showed that the absence of PSA or NCAM delayed migration of neural precursors to the olfactory bulb and consequently enhanced their recruitment at the lesion site. Moreover, after demyelination, the lack of NCAM but not PSA promoted proliferation in the SVZ and the lesion while the lack of PSA favored the differentiation of the traced cells into the oligodendroglial fate both in the SVZ and in the lesion. As previously demonstrated in vitro (L. Decker et al., 2000, Mol. Cell. Neurosci. 16, 422-439), these data illustrate the involvement of PSA and NCAM in neural precursor motility and differentiation in the normal and injured central nervous system, suggesting distinct roles for these two molecules under pathophysiological conditions.
authors.affiliation: INSERM U-546, Laboratoire des Affections la Myéline et des Canaux Ioniques Musculaires, IFRNS, CHU Pitié-Salpêtrière, Paris, France.
authors.forename: Laurence
authors.initials: L
authors.lastname: Decker
authors.forename: Pascale
authors.initials: P
authors.lastname: Durbec
authors.forename: Geneviève
authors.initials: G
authors.lastname: Rougon
authors.forename: Anne
authors.initials: A
authors.lastname: Baron-Van Evercooren
mesh_terms: D000818:Animals; D015703:Antigens, CD / Q000378:metabolism; D001253:Astrocytes / Q000166:cytology / Q000378:metabolism; D051927:CD24 Antigen; D002454:Cell Differentiation / Q000235:genetics*; D002455:Cell Division / Q000235:genetics; D002465:Cell Movement / Q000235:genetics*; D003711:Demyelinating Diseases / Q000139:chemically induced / Q000235:genetics / Q000378:metabolism; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D006026:Glycoside Hydrolases / Q000494:pharmacology; D007150:Immunohistochemistry; D020547:Lateral Ventricles / Q000166:cytology / Q000254:growth & development / Q000378:metabolism; D008244:Lysophosphatidylcholines / Q000494:pharmacology; D008562:Membrane Glycoproteins; D051379:Mice; D018345:Mice, Knockout; D009416:Nerve Regeneration / Q000235:genetics; D019006:Neural Cell Adhesion Molecules / Q000172:deficiency* / Q000235:genetics; D009474:Neurons / Q000378:metabolism*; D012794:Sialic Acids / Q000172:deficiency* / Q000235:genetics; D013234:Stem Cells / Q000166:cytology / Q000378:metabolism*; D013687:Telencephalon / Q000166:cytology / Q000254:growth & development* / Q000378:metabolism
chemical_list: D015703:Antigens, CD; D051927:CD24 Antigen; C497890:Cd24a protein, mouse; D005904:Glial Fibrillary Acidic Protein; D008244:Lysophosphatidylcholines; D008562:Membrane Glycoproteins; D019006:Neural Cell Adhesion Molecules; D012794:Sialic Acids; C021319:polysialic acid; D006026:Glycoside Hydrolases; C090534:endo-alpha-sialidase