Evidence map›Paper›PMID 35075150›Full record

ArticleCell death discovery2022

MicroRNA-181a-2-3p shuttled by mesenchymal stem cell-secreted extracellular vesicles inhibits oxidative stress in Parkinson's disease by inhibiting EGR1 and NOX4.

Jianjun Ma, Xiaoxue Shi, Mingjian Li, Siyuan Chen, Qi Gu, Jinhua Zheng, Dongsheng Li, Shaopu Wu, Hongqi Yang, Xue Li

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 7% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

  1. Pooled it
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  13. Unlocking Parkinson's disease: the role of microRNAs in regulation, diagnosis, and therapy.Apoptosis : an international journal on programmed cell death · 2025
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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

10 authors at 2 institutions in 1 country.

Jianjun MaDepartment of Neurology, Henan Provincial People's Hospital, Zhengzhou, 450003, P. R. China. majj1124@163.com.ORCID http://orcid.org/0000-0001-5825-1927
Xiaoxue ShiDepartment of Neurology, Henan Provincial People's Hospital, Zhengzhou, 450003, P. R. China.
Mingjian LiDepartment of Neurology, Henan Provincial People's Hospital, Zhengzhou, 450003, P. R. China.
Siyuan ChenDepartment of Neurology, Henan Provincial People's Hospital, Zhengzhou, 450003, P. R. China.
Qi GuDepartment of Neurology, Henan Provincial People's Hospital, Zhengzhou, 450003, P. R. China.
Jinhua ZhengDepartment of Neurology, Henan Provincial People's Hospital, Zhengzhou, 450003, P. R. China.
Dongsheng LiDepartment of Neurology, Henan Provincial People's Hospital, Zhengzhou, 450003, P. R. China.
Shaopu WuDepartment of Neurology, Henan Provincial People's Hospital, Zhengzhou, 450003, P. R. China.
Hongqi YangDepartment of Neurology, Henan Provincial People's Hospital, Zhengzhou, 450003, P. R. China.
Xue LiDepartment of Neurology, Henan Provincial People's Hospital, Zhengzhou, 450003, P. R. China.
Zhengzhou University · CNHenan Provincial People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The current study investigated the physiological mechanisms by which extracellular vesicle (EV)-encapsulated miR-181a-2-3p derived from mesenchymal stem cells (MSCs) might mediate oxidative stress (OS) in Parkinson's disease (PD). First, 6-hydroxydopamine (6-OHDA)-induced PD cell and mouse models were established, after which miR-181a-2-3p, EGR1, and NOX4 expression patterns were determined in SH-SY5Y cells and substantia nigra (SN) of PD mice. Next, the binding affinity among miR-181a-2-3p, EGR1, and NOX4 was identified using multiple assays. Gain- or loss-of-function experiments were further adopted to detect SH-SY5Y cell proliferation and apoptosis and to measure the levels of SOD, MDA, and ROS. Finally, the effects of miR-181a-2-3p from MSC-derived EVs in PD mouse models were also explored. It was found that miR-181a-2-3p was poorly expressed in 6-OHDA-induced SH-SY5Y cells, whereas miR-181a-2-3p from MSCs could be transferred into SH-SY5Y cells via EVs. In addition, miR-181a-2-3p could target and inhibit EGR1, which promoted the expression of NOX4. The aforementioned miR-181a-2-3p shuttled by MSC-derived EVs facilitated SH-SY5Y proliferation and SOD levels, but suppressed apoptosis and MDA and ROS levels by regulating EGR1 via inhibition of NOX4/p38 MAPK, so as to repress OS of PD. Furthermore, in PD mice, miR-181a-2-3p was carried by EVs from MSCs to alleviate apoptosis of dopamine neurons and OS, accompanied by increased expressions of α-syn and decreased 4-HNE in SN tissues. Collectively, our findings revealed that MSC-derived EV-loaded miR-181a-2-3p downregulated EGR1 to inhibit OS via the NOX4/p38 MAPK axis in PD.

Identifiers

PMID35075150
PMCPMC8786891
OpenAlexW4206935014

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.