Evidence map›Paper›PMID 37587494›Full record

ArticleCell communication and signaling : CCS2023

Bone mesenchymal stem cell extracellular vesicles delivered miR let-7-5p alleviate endothelial glycocalyx degradation and leakage via targeting ABL2.

Zhe Li, Yuqing Xu, Shiyue Lu, Yuan Gao, Yuxiao Deng

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell communication and signaling : CCS, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 16% 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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. On the road: extracellular vesicles in intercellular communication.Cell communication and signaling : CCS · 2025
    Article
  8. 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

5 authors at 2 institutions in 1 country.

Zhe Li *Department of Critical Care Medicine, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, No. 160, Pujian Road, Pudong New District, Shanghai, 200120, China.
Yuqing Xu *Department of Critical Care Medicine, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, No. 160, Pujian Road, Pudong New District, Shanghai, 200120, China.
Shiyue LuDepartment of Critical Care Medicine, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, No. 160, Pujian Road, Pudong New District, Shanghai, 200120, China.
Yuan GaoDepartment of Critical Care Medicine, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, No. 160, Pujian Road, Pudong New District, Shanghai, 200120, China. rj_gaoyuan@163.com.
Yuxiao DengDepartment of Critical Care Medicine, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, No. 160, Pujian Road, Pudong New District, Shanghai, 200120, China. dengyuxiao@renji.com.
Renji Hospital · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEndothelial glycocalyx (EG) is an active player and treatment target in inflammatory-related vascular leakage. The bone marrow mesenchymal stem cells (bMSCs) are promising potential treatments for leakage; however, the therapeutic effect and mechanism of bMSC on EG degradation needs to be elucidated.

methodsEG degradation and leakage were evaluated in both lipopolysaccharide (LPS)-induced mice ear vascular leakage model and LPS-stimulated human umbilical vein endothelial cells (HUVECs) model treated with bMSCs. Extracellular vesicles (EVs) were extracted from bMSCs and the containing microRNA profile was analyzed. EV and miR let-7-5p were inhibited to determine their function in the therapeutic process. The ABL2 gene was knockdown in HUVECs to verify its role as a therapeutic target in EG degradation.

resultsbMSCs treatment could alleviate LPS-induced EG degradation and leakage in vivo and in vitro, whereas EVs/let-7-5p-deficient bMSCs were insufficient to reduce EG degradation. LPS down-regulated the expression of let-7-5p while upregulated endothelial expression of ABL2 in HUVECs and induced EG degradation and leakage. bMSC-EVs uptaken by HUVECs could deliver let-7-5p targeting endothelial ABL2, which suppressed the activation of downstream p38MAPK and IL-6, IL-1β levels, and thus reversed LPS-induced EG degradation and leakage.

conclusionbMCSs alleviate LPS-induced EG degradation and leakage through EV delivery of miR let-7-5p targeting endothelial ABL2.

Indexed as

Extracellular VesiclesMesenchymal Stem CellsMicroRNAsAnimalsDisease Models, AnimalGlycocalyxHumansHuman Umbilical Vein Endothelial CellsLipopolysaccharidesMiceLipopolysaccharidesMicroRNAsABL2Endothelial glycocalyxExtracellular vesiclesLet-7Mesenchymal stem cells

Identifiers

PMID37587494
PMCPMC10428537
OpenAlexW4385874357

What OpenQuestion 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 OpenQuestion graph.