Circadian control of BDNF-mediated Nrf2 activation in astrocytes protects dopaminergic neurons from ferroptosis.
Animals
Astrocytes
/ metabolism
Brain-Derived Neurotrophic Factor
/ genetics
Circadian Clocks
/ genetics
Dopaminergic Neurons
/ metabolism
Ferroptosis
/ genetics
Iron
/ metabolism
Membrane Glycoproteins
/ genetics
Mice
NF-E2-Related Factor 2
/ genetics
Oxidative Stress
/ genetics
Parkinson Disease
/ genetics
Protein-Tyrosine Kinases
/ genetics
Rats
Rodentia
BDNF
CK2
Circadian rhythm
Cystine transport
Dopamine
Ferroptosis
GSH
Mitochondria
Nrf2
PKA
Parkinson’s disease
TrkB
p75(NTR)
Journal
Free radical biology & medicine
ISSN: 1873-4596
Titre abrégé: Free Radic Biol Med
Pays: United States
ID NLM: 8709159
Informations de publication
Date de publication:
03 2019
03 2019
Historique:
received:
09
07
2018
revised:
20
08
2018
accepted:
01
09
2018
pubmed:
7
9
2018
medline:
15
2
2020
entrez:
7
9
2018
Statut:
ppublish
Résumé
Astrocyte-neuron interactions protect neurons from iron-mediated toxicity. As dopamine can be metabolized to reactive quinones, dopaminergic neurons are susceptible to oxidative damage and ferroptosis-like induced cell death. Detoxification enzymes are required to protect neurons. Brain-derived neurotrophic factor (BDNF) plays a key role in the regulation of redox sensitive transcription factor Nrf2 in astrocytes and metabolic cooperation between astrocytes and neurons. This article reviews the importance of BDNF and astrocyte-neuron interactions in the protection of neurons against oxidative damages in rodent brains. We previously proposed that BDNF activates Nrf2 via the truncated TrkB.T1 and p75
Identifiants
pubmed: 30189266
pii: S0891-5849(18)31523-5
doi: 10.1016/j.freeradbiomed.2018.09.002
pii:
doi:
Substances chimiques
Brain-Derived Neurotrophic Factor
0
Membrane Glycoproteins
0
NF-E2-Related Factor 2
0
Nfe2l2 protein, mouse
0
Iron
E1UOL152H7
Ntrk2 protein, mouse
EC 2.7.10.1
Protein-Tyrosine Kinases
EC 2.7.10.1
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
169-178Subventions
Organisme : British Heart Foundation
ID : FS/15/6/31298
Pays : United Kingdom
Organisme : British Heart Foundation
ID : FS/16/67/32548
Pays : United Kingdom
Organisme : Medical Research Council
Pays : United Kingdom
Informations de copyright
Copyright © 2018 Elsevier Inc. All rights reserved.