Researches of calcium-activated chloride channel ANO1 intervening amyotrophic lateral sclerosis progression by activating EGFR and CaMKII signaling.


Journal

Brain research bulletin
ISSN: 1873-2747
Titre abrégé: Brain Res Bull
Pays: United States
ID NLM: 7605818

Informations de publication

Date de publication:
Nov 2023
Historique:
received: 15 06 2023
revised: 02 10 2023
accepted: 17 10 2023
medline: 27 11 2023
pubmed: 20 10 2023
entrez: 20 10 2023
Statut: ppublish

Résumé

ANO1 is closely correlated with the activation of EGFR and CaMKII, while EGFR and CaMKII show low activation in amyotrophic lateral sclerosis (ALS) models. Therefore, we designed experiments to verify that ANO1 may play a protective role on motor neurons in ALS by activating EGFR and CaMKII. The expression changes of ANO1, EGFR, CaMKII, pEGFR, and pCaMKII, cell survival status, and apoptosis were studied by western blot, real-time quantitative PCR, immunofluorescence, immunohistochemistry, CCK-8, and flow cytometry. The role of ANO1 in the ALS model by activating EGFR and CaMKII was studied by applying corresponding activators, inhibitors, gene silencing, and overexpression. In hSOD1 Our results suggest that ANO1 plays an important role in the survival of ALS motor neurons. ANO1 can increase cell activity and reduce apoptosis by activating EGFR and CaMKII signals.

Sections du résumé

BACKGROUND BACKGROUND
ANO1 is closely correlated with the activation of EGFR and CaMKII, while EGFR and CaMKII show low activation in amyotrophic lateral sclerosis (ALS) models. Therefore, we designed experiments to verify that ANO1 may play a protective role on motor neurons in ALS by activating EGFR and CaMKII.
METHODS METHODS
The expression changes of ANO1, EGFR, CaMKII, pEGFR, and pCaMKII, cell survival status, and apoptosis were studied by western blot, real-time quantitative PCR, immunofluorescence, immunohistochemistry, CCK-8, and flow cytometry. The role of ANO1 in the ALS model by activating EGFR and CaMKII was studied by applying corresponding activators, inhibitors, gene silencing, and overexpression.
RESULTS RESULTS
In hSOD1
CONCLUSIONS CONCLUSIONS
Our results suggest that ANO1 plays an important role in the survival of ALS motor neurons. ANO1 can increase cell activity and reduce apoptosis by activating EGFR and CaMKII signals.

Identifiants

pubmed: 37858681
pii: S0361-9230(23)00217-4
doi: 10.1016/j.brainresbull.2023.110792
pii:
doi:

Substances chimiques

ANO1 protein, mouse 0
Anoctamin-1 0
Calcium-Calmodulin-Dependent Protein Kinase Type 2 EC 2.7.11.17
Chloride Channels 0
ErbB Receptors EC 2.7.10.1
Superoxide Dismutase EC 1.15.1.1
Superoxide Dismutase-1 EC 1.15.1.1
Camk2d protein, mouse EC 2.7.11.17
EGFR protein, mouse EC 2.7.10.1

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

110792

Informations de copyright

Copyright © 2023. Published by Elsevier Inc.

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.

Auteurs

Ying Wang (Y)

Department of Neurology, The First Clinical College of Harbin Medical University, Harbin, China.

Weiwei Liang (W)

Department of Neurology, The First Clinical College of Harbin Medical University, Harbin, China.

Tianhang Wang (T)

Department of Neurology, The First Clinical College of Harbin Medical University, Harbin, China.

Chunting Zhang (C)

Department of Neurology, The First Clinical College of Harbin Medical University, Harbin, China.

Yueqing Yang (Y)

Department of Neurology, The Second Clinical College of Harbin Medical University, Harbin, China.

Chaohua Cong (C)

Department of Neurology, The First Clinical College of Harbin Medical University, Harbin, China.

Xudong Wang (X)

Department of Neurology, The First Clinical College of Harbin Medical University, Harbin, China.

Shuyu Wang (S)

Department of Neurology, The First Clinical College of Harbin Medical University, Harbin, China.

Di Wang (D)

Department of Neurology, The First Clinical College of Harbin Medical University, Harbin, China.

Di Huo (D)

Department of Neurology, The First Clinical College of Harbin Medical University, Harbin, China.

Hongyong Wang (H)

Department of Neurology, The First Clinical College of Harbin Medical University, Harbin, China.

Xiaoli Su (X)

Department of Neurology, The First Clinical College of Harbin Medical University, Harbin, China.

Xingli Tan (X)

Department of Neurology, The First Clinical College of Harbin Medical University, Harbin, China.

Honglin Feng (H)

Department of Neurology, The First Clinical College of Harbin Medical University, Harbin, China. Electronic address: fenghonglin186@sina.com.

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