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論文
タイトル
タイトル(英)
Drug Treatment Attenuates Retinal Ganglion Cell Death by Inhibiting Collapsin Response Mediator Protein 2 Phosphorylation in Mouse Models of Normal Tension Glaucoma.
参照URL
https://researchmap.jp/takayukiharada/published_papers/46402831
著者
著者(英)
Yuebing Wang,Musukha Mala Brahma,Kazuya Takahashi,Alessandra Nolia Blanco Hernandez,Koki Ichikawa,Syuntaro Minami,Yoshio Goshima,Takayuki Harada,Toshio Ohshima
担当区分
概要
概要(英)
Normal tension glaucoma (NTG) is a progressive neurodegenerative disease in glaucoma families. Typical glaucoma develops because of increased intraocular pressure (IOP), whereas NTG develops despite normal IOP. As a subtype of open-angle glaucoma, NTG is characterized by retinal ganglion cell (RGC) degeneration, gradual loss of axons, and injury to the optic nerve. The relationship between glutamate excitotoxicity and oxidative stress has elicited great interest in NTG studies. We recently reported that suppressing collapsin response mediator protein 2 (CRMP2) phosphorylation in S522A CRMP2 mutant (CRMP2 KIKI) mice inhibited RGC death in NTG mouse models. This study evaluated the impact of the natural compounds huperzine A (HupA) and naringenin (NAR), which have therapeutic effects against glutamate excitotoxicity and oxidative stress, on inhibiting CMRP2 phosphorylation in mice intravitreally injected with N-methyl-D-aspartate (NMDA) and GLAST mutant mice. Results of the study demonstrated that HupA and NAR significantly reduced RGC degeneration and thinning of the inner retinal layer, and inhibited the elevated CRMP2 phosphorylation. These treatments protected against glutamate excitotoxicity and suppressed oxidative stress, which could provide insight into developing new effective therapeutic strategies for NTG.
出版者・発行元
出版者・発行元(英)
誌名
誌名(英)
Neuromolecular medicine
26
1
開始ページ
13
終了ページ
13
出版年月
2024年4月15日
査読の有無
招待の有無
掲載種別
研究論文(学術雑誌)
ISSN
DOI URL
https://doi.org/10.1007/s12017-024-08778-1
共同研究・競争的資金等の研究課題
研究者