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  1. C. 医薬保健学域; 医学類・薬学類・医薬科学類・保健学類
  2. c 10. 学術雑誌掲載論文(医・保健)
  3. 1. 査読済論文(医学・保健)

Upregulation of IGF-I in the goldfish retinal ganglion cells during the early stage of optic nerve regeneration

http://hdl.handle.net/2297/18637
http://hdl.handle.net/2297/18637
09987e81-3c3f-4fe2-a6e8-c227dfbf26a9
名前 / ファイル ライセンス アクション
ME-PR-KORIYAMA-Y-749.pdf ME-PR-KORIYAMA-Y-749.pdf (453.8 kB)
Item type 学術雑誌論文 / Journal Article(1)
公開日 2017-10-03
タイトル
タイトル Upregulation of IGF-I in the goldfish retinal ganglion cells during the early stage of optic nerve regeneration
言語
言語 eng
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_6501
資源タイプ journal article
著者 Koriyama, Yoshiki

× Koriyama, Yoshiki

WEKO 332
e-Rad 70397199
研究者番号 70397199

Koriyama, Yoshiki

ja-Kana コオリヤマ, ヨシキ

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Homma, Keiko

× Homma, Keiko

WEKO 21550

Homma, Keiko

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Sugitani, Kayo

× Sugitani, Kayo

WEKO 371
金沢大学研究者情報 20162258
研究者番号 20162258

Sugitani, Kayo

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Higuchi, Yoshihiro

× Higuchi, Yoshihiro

WEKO 21551
e-Rad 10019630
研究者番号 10019630

Higuchi, Yoshihiro

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Matsukawa, Toru

× Matsukawa, Toru

WEKO 379
e-Rad 30219414
研究者番号 30219414

Matsukawa, Toru

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Murayama, Daisuke

× Murayama, Daisuke

WEKO 21552

Murayama, Daisuke

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Kato, Satoru

× Kato, Satoru

WEKO 72
e-Rad 10019614
研究者番号 10019614

Kato, Satoru

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提供者所属
内容記述タイプ Other
内容記述 金沢大学医薬保健研究域 医学系
書誌情報 Neurochemistry International

巻 50, 号 5, p. 749-756, 発行日 2007-04-01
ISSN
収録物識別子タイプ ISSN
収録物識別子 0197-0186
NCID
収録物識別子タイプ NCID
収録物識別子 AA0032399X
DOI
関連タイプ isVersionOf
識別子タイプ DOI
関連識別子 10.1016/j.neuint.2007.01.012
出版者
出版者 Elsevier BV
抄録
内容記述タイプ Abstract
内容記述 Goldfish retinal ganglion cells (RGCs) can regrow their axons after optic nerve injury. However, the reason why goldfish RGCs can regenerate after nerve injury is largely unknown at the molecular level. To investigate regenerative properties of goldfish RGCs, we divided the RGC regeneration process into two components: (1) RGC survival, and (2) axonal elongation processes. To characterize the RGC survival signaling pathway after optic nerve injury, we investigated cell survival/death signals such as Bcl-2 family members in the goldfish retina. Amounts of phospho-Akt (p-Akt) and phospho-Bad (p-Bad) in the goldfish retina rapidly increased four- to five-fold at the protein level by 3-5 days after nerve injury. Subsequently, Bcl-2 levels increased 1.7-fold, accompanied by a slight reduction in caspase-3 activity 10-20 days after injury. Furthermore, level of insulin-like growth factor-I (IGF-I), which activates the phosphatidyl inositol-3-kinase (PI3K)/Akt system, increased 2-3 days earlier than that of p-Akt in the goldfish retina. The cellular localization of these molecular changes was limited to RGCs. IGF-I treatment significantly induced phosphorylation of Akt, and strikingly induced neurite outgrowth in the goldfish retina in vitro. On the contrary, addition of the PI3K inhibitor wortmannin, and IGF-I antibody inhibited Akt phosphorylation and neurite outgrowth in an explant culture. Thus, we demonstrated, for the first time, the signal cascade for early upregulation of IGF-I, leading to RGC survival and axonal regeneration in adult goldfish retinas through PI3K/Akt system after optic nerve injury. The present data strongly indicate that IGF-I is one of the most important molecules for controlling regeneration of RGCs after optic nerve injury. © 2007 Elsevier Ltd. All rights reserved.
著者版フラグ
出版タイプ AM
出版タイプResource http://purl.org/coar/version/c_ab4af688f83e57aa
関連URI
識別子タイプ URI
関連識別子 http://www.elsevier.com/locate/issn/01970186
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