Back to Search Start Over

LncRNA NEAT1 Inhibits Neuronal Apoptosis and Induces Neuronal Viability of Depressed Rats Via microRNA-320-3p/CRHR1 Axis.

Authors :
Huang Y
Jin Y
Yao S
Nan G
Mao Y
Source :
Neurochemical research [Neurochem Res] 2024 Sep; Vol. 49 (9), pp. 2352-2363. Date of Electronic Publication: 2022 Jan 25.
Publication Year :
2024

Abstract

Long noncoding RNA nuclear enriched abundant transcript 1 (NEAT1) has been reported to be involved in depression. This study aims to investigate the mechanism of NEAT1/microRNA (miR)-320-3p/Corticotropin-releasing hormone receptor 1 (CRHR1) axis in depressed rats. Rats with depression-like behaviors were prepared by exposing the rats to chronic unpredictable mild stress. Behavioral functions, pathological damage, neuronal apoptosis and monoamine neurotransmitter were examined in depressed rats . Primary hippocampal neurons were injured through simulation with corticosterone(CORT). Cell viability and apoptosis were measured in CORT-Induced hippocampal neurons. The binding relationship between NEAT1 and miR-320-3p and the targeting relationship between miR-320-3p and CRHR1 were detected. Elevated NEAT1, CRHR1 and reduced miR-320-3p exhibited in depressed rats and CORT-treated hippocampal neurons, NEAT1 bound to miR-320-3p to target CRHR1. Silencing NEAT1 or elevating miR-320-3p improved behavioral functions, attenuated pathological damage and apoptosis in the hippocampus, and increased monoamine neurotransmitter in depressed rats. Repression of NEAT1 or promotion of miR-320-3p enhanced viability and suppressed apoptosis of CORT-treated hippocampal neurons. The study highlights that NEAT1 competitively binds to miR-320-3p to up-regulate CRHR1 expression, thereby promoting hippocampal damage of depressed rats.<br /> (© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Details

Language :
English
ISSN :
1573-6903
Volume :
49
Issue :
9
Database :
MEDLINE
Journal :
Neurochemical research
Publication Type :
Academic Journal
Accession number :
35075548
Full Text :
https://doi.org/10.1007/s11064-021-03508-6