Evidence map›Paper›PMID 34674723›Full record

ArticleJournal of neuroinflammation2021

MicroRNA-204-5p reduction in rat hippocampus contributes to stress-induced pathology via targeting RGS12 signaling pathway.

Tian Lan, Ye Li, Cuiqin Fan, Liyan Wang, Wenjing Wang, Shihong Chen, Shu Yan Yu

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.7field-weighted citation impact, top 19% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

27 citing papers in PubMed, 35 citations in OpenAlex.

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  7. MicroRNAs and synaptic dysfunction in Parkinson's disease.Molecular therapy. Nucleic acids · 2025
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  16. Small Differences and Big Changes: The Many Variables of MicroRNA Expression and Function in the Brain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Tian LanDepartment of Physiology, School of Basic Medical Sciences, Shandong University, 44 Wenhuaxilu Road, Jinan, Shandong, 250012, People's Republic of China.
Ye LiDepartment of Physiology, School of Basic Medical Sciences, Shandong University, 44 Wenhuaxilu Road, Jinan, Shandong, 250012, People's Republic of China.
Cuiqin FanDepartment of Physiology, School of Basic Medical Sciences, Shandong University, 44 Wenhuaxilu Road, Jinan, Shandong, 250012, People's Republic of China.
Liyan WangMorphological Experimental Center, School of Basic Medical Sciences, Shandong University, 44 Wenhuaxilu Road, Jinan, Shandong, 250012, People's Republic of China.
Wenjing WangDepartment of Physiology, School of Basic Medical Sciences, Shandong University, 44 Wenhuaxilu Road, Jinan, Shandong, 250012, People's Republic of China.
Shihong ChenDepartment of Endocrinology, The Second Hospital, Cheeloo College of Medicine, Shandong University, 247 Beiyuan Street, Jinan, Shandong, 250033, People's Republic of China. chenshihong26@163.com.
Shu Yan YuDepartment of Physiology, School of Basic Medical Sciences, Shandong University, 44 Wenhuaxilu Road, Jinan, Shandong, 250012, People's Republic of China. shuyanyu@sdu.edu.cn.ORCID http://orcid.org/0000-0001-6279-1088
Shandong University · CN

Funding

national natural science foundation of china NSFC81873796national natural science foundation of china NSFC82071513natural science foundation of shandong province ZR2020ZD25
6 · The paper itself

Abstract

backgroundNeuroinflammation occupies a pivotal position in the pathogenesis of most nervous system diseases, including depression. However, the underlying molecular mechanisms of neuroinflammation associated with neuronal injury in depression remain largely uncharacterized. Therefore, identifying potential molecular mechanisms and therapeutic targets would serve to better understand the progression of this condition.

methodsChronic unpredictable stress (CUS) was used to induce depression-like behaviors in rats. RNA-sequencing was used to detect the differentially expressed microRNAs. Stereotactic injection of AAV virus to overexpress or knockdown the miR-204-5p. The oxidative markers and inflammatory related proteins were verified by immunoblotting or immunofluorescence assay. The oxidative stress enzyme and products were verified using enzyme-linked assay kit. Electron microscopy analysis was used to observe the synapse and ultrastructural pathology. Finally, electrophysiological recording was used to analyze the synaptic transmission.

resultsHere, we found that the expression of miR-204-5p within the hippocampal dentate gyrus (DG) region of rats was significantly down-regulated after chronic unpredicted stress (CUS), accompanied with the oxidative stress-induced neuronal damage within DG region of these rats. In contrast, overexpression of miR-204-5p within the DG region of CUS rats alleviated oxidative stress and neuroinflammation by directly targeting the regulator of G protein signaling 12 (RGS12), effects which were accompanied with amelioration of depressive-like behaviors in these CUS rats. In addition, down-regulation of miR-204-5p induced neuronal deterioration in DG regions and depressive-like behaviors in rats.

conclusionTaken together, these results suggest that miR-204-5p plays a key role in regulating oxidative stress damage in CUS-induced pathological processes of depression. Such findings provide evidence of the involvement of miR-204-5p in mechanisms underlying oxidative stress associated with depressive phenotype.

Indexed as

AnimalsHippocampusMaleMicroRNAsOrgan Culture TechniquesOxidative StressRatsRats, WistarRGS ProteinsSignal TransductionStress, PsychologicalMicroRNAsMIRN204 microRNA, ratRgs12 protein, ratRGS ProteinsDepressionMiR-204-5pNeuroinflammationOxidative stressRGS12

Identifiers

PMID34674723
PMCPMC8532383
OpenAlexW3206693113

What OpenQuestion holds

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Registered trials

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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 OpenQuestion graph.