Inhibition of death-associated protein kinase 1 attenuates cis P-tau and neurodegeneration in traumatic brain injury.
Cis phosphorylated tau (Cis P-tau)
Cistauosis
Death-associated protein kinase 1 (DAPK1)
Pin1
Traumatic brain injury (TBI)
Journal
Progress in neurobiology
ISSN: 1873-5118
Titre abrégé: Prog Neurobiol
Pays: England
ID NLM: 0370121
Informations de publication
Date de publication:
08 2021
08 2021
Historique:
received:
04
09
2020
revised:
05
04
2021
accepted:
05
05
2021
pubmed:
13
5
2021
medline:
15
2
2022
entrez:
12
5
2021
Statut:
ppublish
Résumé
Traumatic brain injury (TBI) is the leading cause of mortality and disability in young people and may lead to the development of progressive neurodegeneration, such as that observed in chronic traumatic encephalopathy. We have recently found that the conformation-specific cis phosphorylated form of tau (cis P-tau) is a major early driver of neurodegeneration after TBI. However, not much is known about how cis P-tau is regulated in TBI. In this study, we demonstrated a novel critical role of death-associated protein kinase 1 (DAPK1) in regulating cis P-tau induction after TBI. We found that DAPK1 is significantly upregulated in mouse brains after TBI and subsequently promotes cis P-tau induction. Genetic deletion of DAPK1 in mice not only significantly decreases cis P-tau expression, but also effectively attenuates neuropathology development and rescues behavioral impairments after TBI. Mechanistically, DAPK1-mediated cis P-tau induction is regulated by the phosphorylation of Pin1 at Ser71, a unique prolyl isomerase known to control the conformational status of P-tau. Furthermore, pharmacological suppression of DAPK1 kinase activity dramatically decreases the levels of Pin1 phosphorylated at Ser71 as well as cis P-tau after neuronal stress. Thus, DAPK1 is a novel regulator of TBI that, in combination with its downstream targets, has a major impact on the development and/or outcome of TBI, and targeting DAPK1 might offer a potential therapeutic impact on TBI-related neurodegenerative diseases.
Identifiants
pubmed: 33979671
pii: S0301-0082(21)00086-1
doi: 10.1016/j.pneurobio.2021.102072
pmc: PMC8217320
mid: NIHMS1711891
pii:
doi:
Substances chimiques
tau Proteins
0
Dapk1 protein, mouse
EC 2.7.11.1
Death-Associated Protein Kinases
EC 2.7.11.1
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
102072Subventions
Organisme : NIA NIH HHS
ID : R01 AG055559
Pays : United States
Informations de copyright
Copyright © 2021 Elsevier Ltd. All rights reserved.
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