PMID- 18814310
OWN - NLM
STAT- MEDLINE
DCOM- 20090409
LR  - 20120605
IS  - 1932-8451 (Print)
IS  - 1932-8451 (Linking)
VI  - 68
IP  - 13
DP  - 2008 Nov
TI  - A novel role for anosmin-1 in the adhesion and migration of oligodendrocyte 
      precursors.
PG  - 1503-16
LID - 10.1002/dneu.20678 [doi]
AB  - At embryonic stages of development, oligodendrocyte precursors (OPCs) generated 
      in the preoptic area colonize the entire optic nerve (ON). Different factors 
      controlling migration of ON OPCs have been identified, including secreted growth 
      factors, morphogens and guidance cues, as well as cell adhesion molecules. We 
      have shown previously that the soluble form of the extracellular matrix (ECM) 
      protein anosmin-1, impairs OPC migration induced by FGF-2. In the present work, 
      we show that anosmin-1 is expressed by both migrating OPCs and axons of the 
      retinal ganglion cells in the embryonic ON. In vitro, we observe that OPC 
      migration is strongly impaired by contact with anosmin-1 when used as a substrate 
      and, in contrast to previous results, this effect is independent of FGF-2/FGFR1 
      signaling. We also show that OPCs preferentially adhere to anosmin-1 when 
      compared with other ECM molecules used as substrates, and that when the 
      endogenous anosmin-1 expressed by OPCs is blocked, OPC adhesion to all the 
      different substrates (including anosmin-1), is significantly reduced. This novel 
      effect of anosmin-1 on cell adhesion is also independent of FGF-2/FGFR1. We 
      finally demonstrate that the blockade of the endogenous anosmin-1 expressed by 
      OPCs impairs their migration. Our data suggest that the endogenous anosmin-1 
      expressed by OPCs is necessary for the correct adhesion of these cells to the 
      different components of the ECM (including anosmin-1 itself), contributing to the 
      migration of these cells.
CI  - (c) 2008 Wiley Periodicals, Inc.
FAU - Bribian, Ana
AU  - Bribian A
AD  - Grupo de Neurobiologia del Desarrollo-GNDe, Hospital Nacional de Paraplejicos, 
      Finca La Peraleda s/n, Toledo E-45071, Spain.
FAU - Esteban, Pedro F
AU  - Esteban PF
FAU - Clemente, Diego
AU  - Clemente D
FAU - Soussi-Yanicostas, Nadia
AU  - Soussi-Yanicostas N
FAU - Thomas, Jean-Leon
AU  - Thomas JL
FAU - Zalc, Bernard
AU  - Zalc B
FAU - de Castro, Fernando
AU  - de Castro F
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Dev Neurobiol
JT  - Developmental neurobiology
JID - 101300215
RN  - 0 (Antibodies)
RN  - 0 (Chemotactic Factors)
RN  - 0 (Extracellular Matrix Proteins)
RN  - 0 (Gangliosides)
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (ganglioside A2B5)
RN  - 103107-01-3 (Fibroblast Growth Factor 2)
RN  - 9007-34-5 (Collagen)
RN  - EC 2.7.10.1 (Fgfr1 protein, mouse)
RN  - EC 2.7.10.1 (Receptor, Fibroblast Growth Factor, Type 1)
SB  - IM
MH  - Animals
MH  - Animals, Newborn
MH  - Antibodies/pharmacology
MH  - Cell Adhesion/*drug effects/physiology
MH  - Cell Movement/*drug effects/physiology
MH  - Cells, Cultured
MH  - Chemotactic Factors/pharmacology
MH  - Collagen/pharmacology
MH  - Cricetinae
MH  - Cricetulus
MH  - Embryo, Mammalian
MH  - Extracellular Matrix Proteins/genetics/metabolism/*pharmacology
MH  - Fibroblast Growth Factor 2/pharmacology/physiology
MH  - Gangliosides/metabolism
MH  - Gene Expression Regulation, Developmental/physiology
MH  - Mice
MH  - Nerve Tissue Proteins/immunology
MH  - Oligodendroglia/*drug effects/physiology
MH  - RNA, Messenger/metabolism
MH  - Receptor, Fibroblast Growth Factor, Type 1/physiology
MH  - Retina/cytology/embryology/metabolism
MH  - Stem Cells/*drug effects/physiology
EDAT- 2008/09/25 09:00
MHDA- 2009/04/10 09:00
CRDT- 2008/09/25 09:00
PHST- 2008/09/25 09:00 [pubmed]
PHST- 2009/04/10 09:00 [medline]
PHST- 2008/09/25 09:00 [entrez]
AID - 10.1002/dneu.20678 [doi]
PST - ppublish
SO  - Dev Neurobiol. 2008 Nov;68(13):1503-16. doi: 10.1002/dneu.20678.