Sestrin2 overexpression alleviates hydrogen peroxide-induced apoptosis and oxidative stress in retinal ganglion cells by enhancing Nrf2 activation via Keap1 downregulation.
Animals
Antioxidant Response Elements
/ physiology
Apoptosis
/ drug effects
Down-Regulation
Hydrogen Peroxide
/ pharmacology
Kelch-Like ECH-Associated Protein 1
/ metabolism
NF-E2-Related Factor 2
/ metabolism
Nuclear Proteins
/ metabolism
Oxidative Stress
/ drug effects
Rats
Retinal Ganglion Cells
/ drug effects
Signal Transduction
/ drug effects
Up-Regulation
Glaucoma
Keap1
Nrf2
Retinal ganglion cells
Sesn2
Journal
Chemico-biological interactions
ISSN: 1872-7786
Titre abrégé: Chem Biol Interact
Pays: Ireland
ID NLM: 0227276
Informations de publication
Date de publication:
01 Jun 2020
01 Jun 2020
Historique:
received:
15
01
2020
revised:
17
03
2020
accepted:
02
04
2020
pubmed:
11
4
2020
medline:
27
5
2020
entrez:
11
4
2020
Statut:
ppublish
Résumé
Oxidative stress-induced apoptosis of retinal ganglion cells (RGCs) contributes to the development and progression of glaucoma. Sestrin2 (Sesn2), a stress-inducible protein, has a potent antioxidant capacity that can provide cytoprotection against various noxious stimuli. However, whether Sesn2 is involved in protecting RGCs from oxidative stress remains unexplored. The purpose of this study was to evaluate the role of Sesn2 in regulating hydrogen peroxide (H
Identifiants
pubmed: 32275923
pii: S0009-2797(20)30078-8
doi: 10.1016/j.cbi.2020.109086
pii:
doi:
Substances chimiques
KEAP1 protein, rat
0
Kelch-Like ECH-Associated Protein 1
0
NF-E2-Related Factor 2
0
Nfe2l2 protein, rat
0
Nuclear Proteins
0
Sesn2 protein, rat
0
Hydrogen Peroxide
BBX060AN9V
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
109086Informations de copyright
Copyright © 2020 Elsevier B.V. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.