Neuronal and glial expression of the adhesion molecule TAG-1 is regulated after peripheral nerve lesion or central neurodegeneration of adult nervous system.
Expression of the cell adhesion molecule TAG-1 is down-regulated in adult brain, with the exception of certain areas exhibiting structural plasticity. Here, we present evidence that TAG-1 expression persists also in adult rat spinal cord and dorsal root ganglia (DRG), and can be up-regulated after injury. On Western blots of adult tissue, TAG-1 is detected as a 135-kDa band, with an additional specific 90-kDa band, not present in developing tissue. TAG-1 expression is found both in DRG neurons and in Schwann cells, particularly those associated with the peripherally projecting DRG processes. Quantitative in situ hybridization revealed that TAG-1 expression is significantly higher in small neurons that give rise to unmyelinated fibers, than in large DRG neurons. The regulation of TAG-1 was then examined in two different lesion paradigms. After a sciatic nerve lesion, TAG-1 expression is not up-regulated in DRG neurons, but decreases with time. At the lesion site, reactive Schwann cells up-regulate TAG-1, as demonstrated by both immunohistochemistry and in situ hybridization. In a second paradigm, we injected kainic acid into the spinal cord that kills neurons but spares glia and axons. TAG-1 is up-regulated in the spinal neuron-depleted area as well as in the corresponding dorsal and ventral roots, associated with both target-deprived afferent fibers and with the non-neuronal cells that invade the lesion site. These results demonstrate a local up-regulation of TAG-1 in the adult that is induced in response to injury, suggesting its involvement in axonal re-modelling, neuron-glia interactions, and glial cell migration.
Soares
Sylvia
S
Laboratoire de Neurobiologie des Signaux Intercellulaires, UMR7101, CNRS-UPMC, Case 02, Bat. A, 3étage, 7 Quai Saint Bernard, 75005 Paris, France.
Traka
Maria
M
von Boxberg
Ysander
Y
Bouquet
Céline
C
Karagogeos
Domna
D
Nothias
Fatiha
F
D000818:Animals; D000831:Animals, Newborn; D015153:Blotting, Western / Q000379:methods; D015816:Cell Adhesion Molecules, Neuronal / Q000235:genetics / Q000378:metabolism*; D002478:Cells, Cultured; D058969:Contactin 2; D004268:DNA-Binding Proteins / Q000378:metabolism; D051767:Early Growth Response Protein 2; D005260:Female; D005727:Ganglia, Spinal / Q000166:cytology / Q000254:growth & development / Q000378:metabolism; D018507:Gene Expression Regulation, Developmental / Q000502:physiology; D007150:Immunohistochemistry / Q000379:methods; D017403:In Situ Hybridization / Q000379:methods; D007211:Indoles / Q000378:metabolism; D007608:Kainic Acid; D008869:Microtubule-Associated Proteins / Q000378:metabolism; D009410:Nerve Degeneration / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology; D009457:Neuroglia / Q000378:metabolism*; D009474:Neurons / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D009418:S100 Proteins / Q000378:metabolism; D012583:Schwann Cells; D020426:Sciatic Neuropathy / Q000378:metabolism*; D013116:Spinal Cord / Q000166:cytology / Q000254:growth & development / Q000378:metabolism; D014157:Transcription Factors / Q000378:metabolism
D015816:Cell Adhesion Molecules, Neuronal; C548676:Cntn2 protein, rat; D058969:Contactin 2; D004268:DNA-Binding Proteins; D051767:Early Growth Response Protein 2; C497328:Egr2 protein, rat; D007211:Indoles; D008869:Microtubule-Associated Proteins; D012333:RNA, Messenger; D009418:S100 Proteins; D014157:Transcription Factors; C085284:microtubule-associated protein 1B; C007293:DAPI; D007608:Kainic Acid