N


Journal

Biological psychiatry
ISSN: 1873-2402
Titre abrégé: Biol Psychiatry
Pays: United States
ID NLM: 0213264

Informations de publication

Date de publication:
01 09 2020
Historique:
received: 15 08 2019
revised: 14 02 2020
accepted: 18 02 2020
pubmed: 11 5 2020
medline: 20 2 2021
entrez: 11 5 2020
Statut: ppublish

Résumé

N Circular RNA STAG1 (circSTAG1) was screened from the hippocampus of chronic unpredictable stress-treated mice using high-throughput RNA sequencing. Microinjection of circSTAG1 lentivirus into the mouse hippocampus was used to observe the role of circSTAG1 in depression. Sucrose preference, forced swim, and tail suspension tests were performed to evaluate the depressive-like behaviors of mice. Astrocyte dysfunction was examined by GFAP immunostaining and 3D reconstruction. Methylated RNA immunoprecipitation sequence analysis was used to identify downstream targets of circSTAG1/ALKBH5 (alkB homolog 5) axis. Cell Counting Kit-8 assay was performed to evaluate astrocyte viability in vitro. circSTAG1 was significantly decreased in the chronic unpredictable stress-treated mouse hippocampus and in peripheral blood of patients with MDD. Overexpression of circSTAG1 notably attenuated astrocyte dysfunction and depressive-like behaviors induced by chronic unpredictable stress. Further examination indicated that overexpressed circSTAG1 captured ALKBH5 and decreased the translocation of ALKBH5 into the nucleus, leading to increased m Our findings dissect the functional link between circSTAG1 and m

Sections du résumé

BACKGROUND
N
METHODS
Circular RNA STAG1 (circSTAG1) was screened from the hippocampus of chronic unpredictable stress-treated mice using high-throughput RNA sequencing. Microinjection of circSTAG1 lentivirus into the mouse hippocampus was used to observe the role of circSTAG1 in depression. Sucrose preference, forced swim, and tail suspension tests were performed to evaluate the depressive-like behaviors of mice. Astrocyte dysfunction was examined by GFAP immunostaining and 3D reconstruction. Methylated RNA immunoprecipitation sequence analysis was used to identify downstream targets of circSTAG1/ALKBH5 (alkB homolog 5) axis. Cell Counting Kit-8 assay was performed to evaluate astrocyte viability in vitro.
RESULTS
circSTAG1 was significantly decreased in the chronic unpredictable stress-treated mouse hippocampus and in peripheral blood of patients with MDD. Overexpression of circSTAG1 notably attenuated astrocyte dysfunction and depressive-like behaviors induced by chronic unpredictable stress. Further examination indicated that overexpressed circSTAG1 captured ALKBH5 and decreased the translocation of ALKBH5 into the nucleus, leading to increased m
CONCLUSIONS
Our findings dissect the functional link between circSTAG1 and m

Identifiants

pubmed: 32387133
pii: S0006-3223(20)30113-X
doi: 10.1016/j.biopsych.2020.02.018
pii:
doi:

Substances chimiques

Nuclear Proteins 0
RNA, Circular 0
RNA, Messenger 0
STAG1 protein, human 0
N-methyladenosine CLE6G00625
Amidohydrolases EC 3.5.-
fatty-acid amide hydrolase EC 3.5.1.-
Adenosine K72T3FS567

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

392-404

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2020 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.

Auteurs

Rongrong Huang (R)

Department of Pharmacology, School of Medicine, Southeast University, Nanjing, China.

Yuan Zhang (Y)

Department of Pharmacology, School of Medicine, Southeast University, Nanjing, China.

Ying Bai (Y)

Department of Pharmacology, School of Medicine, Southeast University, Nanjing, China.

Bing Han (B)

Department of Pharmacology, School of Medicine, Southeast University, Nanjing, China.

Minzi Ju (M)

Department of Pharmacology, School of Medicine, Southeast University, Nanjing, China.

Biling Chen (B)

Department of Pharmacology, School of Medicine, Southeast University, Nanjing, China.

Li Yang (L)

Department of Pharmacology, School of Medicine, Southeast University, Nanjing, China.

Yu Wang (Y)

Department of Pharmacology, School of Medicine, Southeast University, Nanjing, China.

Hongxing Zhang (H)

Department of Psychology, Xinxiang Medical University, Xinxiang, Henan, China; Second Affiliated Hospital, Xinxiang Medical University, Xinxiang, Henan, China.

Haisan Zhang (H)

Second Affiliated Hospital, Xinxiang Medical University, Xinxiang, Henan, China.

Chunming Xie (C)

Department of Neurology, Affiliated ZhongDa Hospital, Institute of Neuropsychiatry, Southeast University, Nanjing, China.

Zhijun Zhang (Z)

Department of Neurology, Affiliated ZhongDa Hospital, Institute of Neuropsychiatry, Southeast University, Nanjing, China; Department of Psychology, Xinxiang Medical University, Xinxiang, Henan, China; Second Affiliated Hospital, Xinxiang Medical University, Xinxiang, Henan, China.

Honghong Yao (H)

Department of Pharmacology, School of Medicine, Southeast University, Nanjing, China; Institute of Life Sciences, Key Laboratory of Developmental Genes and Human Disease, Southeast University, Nanjing, China; Co-innovation Center of Neuroregeneration, Nantong University, Nantong, Jiangsu, China. Electronic address: yaohh@seu.edu.cn.

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Classifications MeSH