Artigo Revisado por pares

Adenoviral gene transfer of GDNF, BDNF and TGFβ2, but not CNTF, cardiotrophin‐1 or IGF1, protects injured adult motoneurons after facial nerve avulsion

2003; Wiley; Volume: 72; Issue: 1 Linguagem: Inglês

10.1002/jnr.10558

ISSN

1097-4547

Autores

Tsuyoshi Sakamoto, Yoko Kawazoe, Jin‐Song Shen, Yasuo Takeda, Yoshihiro Arakawa, Junko Ogawa, Kiyomitsu Oyanagi, Toya Ohashi, Kazutada Watanabe, Kiyoharu Inoue, Yoshikatsu Eto, Kazuhiko Watabe,

Tópico(s)

Neurogenesis and neuroplasticity mechanisms

Resumo

Abstract We examined neuroprotective effects of recombinant adenoviral vectors encoding glial cell line‐derived neurotrophic factor (GDNF), brain‐derived neurotrophic factor (BDNF), ciliary neurotrophic factor (CNTF), cardiotrophin‐1 (CT1), insulin‐like growth factor‐1 (IGF1), and transforming growth factor‐β2 (TGFβ2) on lesioned adult rat facial motoneurons. The right facial nerves of adult Fischer 344 male rats were avulsed and removed from the stylomastoid foramen, and adenoviral vectors were injected into the facial canal. Animals avulsed and treated with adenovirus encoding GDNF, BDNF, CNTF, CT1, IGF1 and TGFβ2 showed intense immunolabeling for these factors in lesioned facial motoneurons, respectively, indicating adenoviral induction of the neurotrophic factors in these neurons. The treatment with adenovirus encoding GDNF, BDNF, or TGFβ2 after avulsion significantly prevented the loss of lesioned facial motoneurons, improved choline acetyltransferase immunoreactivity and prevented the induction of nitric oxide synthase activity in these neurons. The treatment with adenovirus encoding CNTF, CT1 or IGF1, however, failed to protect these neurons after avulsion. These results indicate that the gene transfer of GDNF and BDNF and TGFβ2 but not CNTF, CT1 or IGF1 may prevent the degeneration of motoneurons in adult humans with motoneuron injury and motor neuron diseases. © 2003 Wiley‐Liss, Inc.

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