Artemin augments survival and axon regeneration in axotomized retinal ganglion cells

Kazuko Omodaka, Takuji Kurimoto, Orie Nakamura, Kota Sato, Masayuki Yasuda, Yuji Tanaka, Noriko Himori, Yu Yokoyama, Toru Nakazawa

研究成果: Article査読

10 被引用数 (Scopus)

抄録

Artemin, a recently discovered member of the glial cell line-derived neurotrophic factor (GDNF) family, has neurotrophic effects on damaged neurons, including sympathetic neurons, dopamine neurons, and spiral ganglion neurons both in vivo and in vitro. However, its effects on retinal cells and its intracellular signaling remain relatively unexplored. During development, expression of GFRα3, a specific receptor for artemin, is strong in the immature retina and gradually decreases during maturation, suggesting a possible role in the formation of retinal connections. Optic nerve damage in mature rats causes levels of GFRα3 mRNA to increase tenfold in the retina within 3 days. GFRα3 mRNA levels continue to rise within the first week and then decline. Artemin, a specific ligand for GFRα3, has a neuroprotective effect on axotomized retinal ganglion cells (RGCs) in vivo and in vitro via activation of the extracellular signal-related kinase- and phosphoinositide 3-kinase-Akt signaling pathways. Artemin also has a substantial effect on axon regeneration in RGCs both in vivo and in vitro, whereas other GDNF family members do not. Therefore, artemin/GFRα3, but not other GDNF family members, may be of value for optic nerve regeneration in mature mammals.

本文言語English
ページ(範囲)1637-1646
ページ数10
ジャーナルJournal of Neuroscience Research
92
12
DOI
出版ステータスPublished - 2014 12 1

ASJC Scopus subject areas

  • 細胞および分子神経科学

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