ArticleExperimental brain research2021
MiR-129-5p prevents depressive-like behaviors by targeting MAPK1 to suppress inflammation.
Article in Experimental brain research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- Peripheral miRNA profiling identifies therapy-specific biological trajectories in the treatment of cognitive dysfunction in depression: an exploratory mechanistic study.Scientific reports · 2026Trial
- Changes in Multiple microRNA Levels with Antidepressant Treatment Are Associated with Remission and Interact with Key Pathways: A Comprehensive microRNA Analysis.International journal of molecular sciences · 2023Trial
- Sex-Specific Hippocampal Phosphoproteomic Features Associated with Stress-Induced Phenotypes in Mice Exposed to Chronic Restraint Stress.Neurochemical research · 2026Article
- MicroRNA-129-5p in the mPFC is involved in the chronic mild stress-induced depression-like behaviors in rats.Acta pharmacologica Sinica · 2026Article
- A ferroptosis-related competing endogenous RNA network: HOX transcript antisense intergenic RNA/miR-129-5p/brain and acute leukemia, cytoplasmic axis contributes to the malignant progression of esophageal squamous cell carcinoma.Translational cancer research · 2026Article
- Effects of the LINC00641/miR-323a-3p/EIF4G2 axis on behaviors and brain monoamine neurotransmitters in chronic unpredictable mild stress mice.Cell biology and toxicology · 2025Article
- MiR-129-5p alleviates depression and anxiety by increasing astrocyte ATP production partly through targeting deubiquitinase Mysm1.PloS one · 2025Article
- Profiling Small RNA From Brain Extracellular Vesicles in Individuals With Depression.The international journal of neuropsychopharmacology · 2024Article
- Mechanism ofCurrent computer-aided drug design · 2024Article
- Integrating network pharmacology with molecular docking to rationalize the ethnomedicinal use ofFrontiers in pharmacology · 2024Article
- Amalgamated Pharmacoinformatics Study to Investigate the Mechanism of Xiao Jianzhong Tang against Chronic Atrophic Gastritis.Current computer-aided drug design · 2024Article
- Chronic stress and stressful emotional contagion affect the empathy-like behavior of rats.Cognitive, affective & behavioral neuroscience · 2023Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Depression is a complex etiological disease with limited effective treatments. Previous studies have indicated the involvement of miRNAs in the pathophysiology of mood disorders. In this study, we focused on the role and mechanisms of miR-129-5p in depression by successfully constructing mice models of depressive-like behavior via chronic unpredictable mild stress (CUMS) exposure. Herein, miR-129-5p expression was decreased in the hippocampus of CUMS mice model. Upregulation of miR-129-5p reduced depressive-like behaviors of CUMS mice, as revealed in sucrose preference test, novelty suppressed feeding test, forced swim test, tail suspension test, social interaction test. MiR-129-5p upregulation decreased the concentrations and protein levels of proinflammatory cytokines (IL-6, IL-1β and TNF-α), indicating the inhibitory role of miR-129-5p in inflammation. Furthermore, miR-129-5p was identified to target MAPK1. MAPK1 was negatively regulated by miR-129-5p, and silencing of MAPK1 attenuated depressive-like behaviors in CUMS mice. Moreover, MAPK1 downregulation decreased inflammation in the hippocampus of CUMS mice. Upregulation of MAPK1 reversed the suppressive effects of miR-129-5p upregulation on depressive-like behaviors and inflammation in CUMS mice. In conclusion, the current study identified that miR-129-5p reduces depressive-like behaviors and suppresses inflammation by targeting MAPK1 in CUMS mice, offering a novel molecular interpretation for depression prevention.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.