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Neurotrophin expression in neural stem cells grafted acutely to transected spinal cord of adult rats linked to functional improvement.
Gu, Ying-Li; Yin, Lu-Wei; Zhang, Zhuo; Liu, Jia; Liu, Su-Juan; Zhang, Lian-Feng; Wang, Ting-Hua.
Afiliação
  • Gu YL; Department of Neurology, West China Hospital, Sichuan University, Chengdu, China.
Cell Mol Neurobiol ; 32(7): 1089-97, 2012 Oct.
Article em En | MEDLINE | ID: mdl-22573254
ABSTRACT
It is well known that neural stem cells (NSC) could promote the repairment after spinal cord injury, but the underlying mechanism remains to be elucidated. This study showed that the transplantation of NSC significantly improved hindlimb locomotor functions in adult rats subjected to transection of the spinal cord. Biotin dextran amine tracing together with the stimulus experiment in motor sensory area showed that little CST regeneration existed and functional synaptic formation in the injury site. Immunocytochemistry and RT-PCR demonstrated the secretion of NGF, BDNF, and NT-3 by NSC in vitro and in vivo, respectively. However, only mRNA expression of BDNF and NT-3 but not NGF in injury segment following NSC transplantation was upregulated remarkably, while caspase-3, a crucial apoptosis gene, was downregulated simultaneously. These provided us a clue that the functional recovery was correlated with the regulation of BDNF, NT-3, and caspase-3 in spinal cord transected rats following NSC transplantation.
Assuntos
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Base de dados: MEDLINE Assunto principal: Traumatismos da Medula Espinal / Fator Neurotrófico Derivado do Encéfalo / Recuperação de Função Fisiológica / Neurotrofina 3 / Transplante de Células-Tronco / Células-Tronco Neurais Limite: Animals Idioma: En Ano de publicação: 2012 Tipo de documento: Article
Buscar no Google
Base de dados: MEDLINE Assunto principal: Traumatismos da Medula Espinal / Fator Neurotrófico Derivado do Encéfalo / Recuperação de Função Fisiológica / Neurotrofina 3 / Transplante de Células-Tronco / Células-Tronco Neurais Limite: Animals Idioma: En Ano de publicação: 2012 Tipo de documento: Article