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Cloning and expression of a retinoic acid receptor ß2 subtype from the adult newt: evidence for an early role in tail and caudal spinal cord regeneration.
Carter, Christopher; Clark, Alysen; Spencer, Gaynor; Carlone, Robert.
Afiliação
  • Carter C; Department of Biological Sciences, Brock University, 500 Glenridge Avenue, St. Catharines, Ontario, Canada.
Dev Dyn ; 240(12): 2613-25, 2011 Dec.
Article em En | MEDLINE | ID: mdl-22052812
ABSTRACT
Retinoic acid receptor beta 2 (RARß2) has been proposed as an important receptor mediating retinoid-induced axonal growth and regeneration in developing mammalian spinal cord and brain. In urodele amphibians, organisms capable of extensive central nervous system (CNS) regeneration as adults, this receptor had not been isolated, nor had its function been characterized. We have cloned a full-length RARß2 cDNA from adult newt CNS. This receptor, NvRARß2, is expressed in various adult organs capable of regeneration, including the spinal cord. Interestingly, both the NvRARß2 mRNA and protein are up-regulated during the first 2 weeks after amputation of the tail, primarily in the ependymoglial and meningeal tissues near the rostral cut surface of the cord. Treatment with LE135, a RARß-selective antagonist, caused a significant inhibition of ependymal outgrowth and a decrease in tail regenerate length. These data support an early role for this receptor in caudal spinal cord and tail regeneration in this amphibian.
Assuntos

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Regeneração / Medula Espinal / Cauda / Regulação da Expressão Gênica / Receptores do Ácido Retinoico / Proteínas de Anfíbios Limite: Animals / Humans Idioma: En Ano de publicação: 2011 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Regeneração / Medula Espinal / Cauda / Regulação da Expressão Gênica / Receptores do Ácido Retinoico / Proteínas de Anfíbios Limite: Animals / Humans Idioma: En Ano de publicação: 2011 Tipo de documento: Article