Evidence map›Paper›PMID 32745988›Full record

ArticleiScience2020

Down-Regulation of miR-301a-3p Reduces Burn-Induced Vascular Endothelial Apoptosis by potentiating hMSC-Secreted IGF-1 and PI3K/Akt/FOXO3a Pathway.

Lingying Liu, Huinan Yin, Xingxia Hao, Huifeng Song, Jiake Chai, Hongjie Duan, Yang Chang, Longlong Yang, Yushou Wu, Shaofang Han and 9 more

Abstract read
In one paragraph

Article in iScience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
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

12 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. MicroRNA Profiles in Critically Ill Patients.Current medicinal chemistry · 2024
    Review
  5. Review
  6. Molecular mechanisms of cell death in bronchopulmonary dysplasia.Apoptosis : an international journal on programmed cell death · 2023
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
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

19 authors.

Lingying LiuNutrition Department, the Fourth Medical Center Affiliated to PLA General Hospital, Beijing 100037, China; Burns Institute of PLA, Department of Burn & Plastic Surgery, the Fourth Medical Center Affiliated to PLA General Hospital, Beijing 100037, China; College of Basic Medicine, the Inner Mongolia Medical University, Hohhot, 010110, Inner Mongolia, China.
Huinan YinBurns Institute of PLA, Department of Burn & Plastic Surgery, the Fourth Medical Center Affiliated to PLA General Hospital, Beijing 100037, China.
Xingxia HaoCollege of Basic Medicine, the Inner Mongolia Medical University, Hohhot, 010110, Inner Mongolia, China.
Huifeng SongBurns Institute of PLA, Department of Burn & Plastic Surgery, the Fourth Medical Center Affiliated to PLA General Hospital, Beijing 100037, China.
Jiake ChaiBurns Institute of PLA, Department of Burn & Plastic Surgery, the Fourth Medical Center Affiliated to PLA General Hospital, Beijing 100037, China. Electronic address: cjk304@126.com.
Hongjie DuanBurns Institute of PLA, Department of Burn & Plastic Surgery, the Fourth Medical Center Affiliated to PLA General Hospital, Beijing 100037, China.
Yang ChangBurns Institute of PLA, Department of Burn & Plastic Surgery, the Fourth Medical Center Affiliated to PLA General Hospital, Beijing 100037, China.
Longlong YangBurns Institute of PLA, Department of Burn & Plastic Surgery, the Fourth Medical Center Affiliated to PLA General Hospital, Beijing 100037, China.
Yushou WuBurns Institute of PLA, Department of Burn & Plastic Surgery, the Fourth Medical Center Affiliated to PLA General Hospital, Beijing 100037, China.
Shaofang HanBurns Institute of PLA, Department of Burn & Plastic Surgery, the Fourth Medical Center Affiliated to PLA General Hospital, Beijing 100037, China.
Xiaoteng WangBurns Institute of PLA, Department of Burn & Plastic Surgery, the Fourth Medical Center Affiliated to PLA General Hospital, Beijing 100037, China.
Xiaotong YueBurns Institute of PLA, Department of Burn & Plastic Surgery, the Fourth Medical Center Affiliated to PLA General Hospital, Beijing 100037, China.
Yunfei ChiBurns Institute of PLA, Department of Burn & Plastic Surgery, the Fourth Medical Center Affiliated to PLA General Hospital, Beijing 100037, China.
Wei LiuBurns Institute of PLA, Department of Burn & Plastic Surgery, the Fourth Medical Center Affiliated to PLA General Hospital, Beijing 100037, China.
Qiong WangDepartment of Burn Surgery, the Third Affiliated Hospital of Inner Mongolia Medical University (Inner Mongolia BaoGang Hospital), Baotou 014010, Inner Mongolia, China.
Hongyu WangDepartment of Burn Surgery, the Third Affiliated Hospital of Inner Mongolia Medical University (Inner Mongolia BaoGang Hospital), Baotou 014010, Inner Mongolia, China.
Hailiang BaiDepartment of Plastic Surgery, The Second Hospital, Shanxi Medical University, Taiyuan 030001, Shanxi Province, China.
Xiuxiu ShiDepartment of Orthopedic Rehabilitation, the Fourth Medical Center Affiliated to PLA General Hospital, Beijing, 100037, China.
Shaozeng LiDepartment of Clinical Laboratory, the Fourth Medical Center Affiliated to PLA General Hospital, Beijing 100037, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vascular endothelium dysfunction plays a pivotal role in the initiation and progression of multiple organ dysfunction. The mesenchymal stem cell (MSC) maintains vascular endothelial barrier survival via secreting bioactive factors. However, the mechanism of human umbilical cord MSC (hMSC) in protecting endothelial survival remains unclear. Here, we found IGF-1 secreted by hMSC suppressed severe burn-induced apoptosis of human umbilical vein endothelial cells (HUVECs) and alleviated the dysfunction of vascular endothelial barrier and multiple organs in severely burned rats. Severe burn repressed miR-301a-3p expression, which directly regulated IGF-1 synthesis and secretion in hMSC. Down-regulation of miR-301a-3p decreased HUVECs apoptosis, stabilized endothelial barrier permeability, and subsequently protected against multiple organ dysfunction in vivo. Additionally, miR-301a-3p negatively regulated PI3K/Akt/FOXO3 signaling through IGF-1. Taken together, our study highlights the protective function of IGF-1 against the dysfunction of multiple organs negatively regulated by miR-301a-3p, which may provide the theoretical foundation for further clinical application of hMSC.

Indexed as

Cellular TherapyClinical GeneticsStem Cells Research

Identifiers

PMID32745988
PMCPMC7399190

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.