Evidence map›Paper›PMID 34230646›Full record

ArticleLaboratory investigation; a journal of technical methods and pathology2021

M1 macrophage-derived exosomes transfer miR-222 to induce bone marrow mesenchymal stem cell apoptosis.

Yanyan Qi, Tingting Zhu, Tingting Zhang, Xi Wang, Wenbo Li, Dongchang Chen, Hua Meng, Songtao An

Erratum issuedOpen access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Laboratory investigation; a journal of technical methods and pathology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
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

33 citing papers in PubMed, 50 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Yanyan QiDepartment of Cardiology, Henan Provincial People's Hospital, Zhengzhou University People's Hospital, 7 Weiwu Road, Zhengzhou, China.
Tingting ZhuDepartment of Cardiology, Henan Provincial People's Hospital, Zhengzhou University People's Hospital, 7 Weiwu Road, Zhengzhou, China.
Tingting ZhangDepartment of Cardiology, Henan Provincial People's Hospital, Zhengzhou University People's Hospital, 7 Weiwu Road, Zhengzhou, China.
Xi WangDepartment of Cardiology, Henan Provincial People's Hospital, Zhengzhou University People's Hospital, 7 Weiwu Road, Zhengzhou, China.
Wenbo LiDepartment of Cardiology, Henan Provincial People's Hospital, Zhengzhou University People's Hospital, 7 Weiwu Road, Zhengzhou, China.
Dongchang ChenDepartment of Cardiology, Henan Provincial People's Hospital, Zhengzhou University People's Hospital, 7 Weiwu Road, Zhengzhou, China.
Hua MengDepartment of Cardiology, Henan Provincial People's Hospital, Zhengzhou University People's Hospital, 7 Weiwu Road, Zhengzhou, China.
Songtao AnDepartment of Cardiology, Henan Provincial People's Hospital, Zhengzhou University People's Hospital, 7 Weiwu Road, Zhengzhou, China. ansongtao2020@163.com.
Henan Provincial People's Hospital · CNZhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the myocardial infarction microenvironment, the effect of macrophages on the function of bone marrow mesenchymal stem cells (BMSCs) is unclear. In this study, we investigated the role of hypoxia/serum deprivation (H/SD)-induced M1-type macrophage-derived exosomes on BMSC viability, migration, and apoptosis. We found that H/SD reduced BMSC viability and migration, increased BMSC apoptosis, and induced macrophage polarization toward the M1 phenotype. BMSCs were cultured by the supernatant of H/SD-induced THP-1 cells (M1-type macrophages) with or without exosome inhibitor treatment. The results show that BMSC apoptosis is increased in the H/SD-induced THP-1 cell supernatant group and is decreased by GM4869 treatment, indicating that M1-type macrophages induce BMSC apoptosis through exosomes. In addition, we confirm that miR-222 plays an important role in promoting BMSC apoptosis by targeting B-cell lymphoma (Bcl)-2. M1-type macrophage-derived exosomes significantly decrease BMSC viability and migration and increase BMSC apoptosis, and these effects are partly abolished by a miR-222 inhibitor. Our findings suggest that under H/SD conditions, exosomes derived from M1-type macrophages can induce BMSC apoptosis by delivering miR-222 to BMSCs.

Indexed as

ExosomesMacrophagesMesenchymal Stem CellsApoptosisCell HypoxiaCells, CulturedCell SurvivalHumansMicroRNAsMicroRNAsMIR222, human

Identifiers

PMID34230646
OpenAlexW3182079070

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.