Evidence map›Paper›PMID 31878977›Full record

ArticleJournal of translational medicine2019

The regulatory effect of microRNA-21a-3p on the promotion of telocyte angiogenesis mediated by PI3K (p110α)/AKT/mTOR in LPS induced mice ARDS.

Yile Zhou, Yajie Yang, Tao Liang, Yan Hu, Haihong Tang, Dongli Song, Hao Fang

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 18% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

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  20. Cd34+ Stromal Cells/Telocytes in Normal and Pathological Skin.International journal of molecular sciences · 2021
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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 3 institutions in 1 country.

Yile ZhouDepartment of Anaesthesiology, Jinshan Hospital, Fudan University, 1508 Longhang Road, Shanghai, 201508, People's Republic of China.
Yajie YangDepartment of Anaesthesiology, Jinshan Hospital, Fudan University, 1508 Longhang Road, Shanghai, 201508, People's Republic of China.
Tao LiangDepartment of Anaesthesiology, Jinshan Hospital, Fudan University, 1508 Longhang Road, Shanghai, 201508, People's Republic of China.
Yan HuDepartment of Anaesthesiology, Jinshan Hospital, Fudan University, 1508 Longhang Road, Shanghai, 201508, People's Republic of China.
Haihong TangDepartment of Anaesthesiology, Jinshan Hospital, Fudan University, 1508 Longhang Road, Shanghai, 201508, People's Republic of China.
Dongli SongZhongshan Hospital Institute for Clinical Science, Shanghai Institute of Clinical Bioinformatics, Shanghai Engineering Research for AI Technology for Cardiopulmonary Diseases, Shanghai Medical College, Fudan University, Shanghai, China. songdongli37@126.com.
Hao FangDepartment of Anaesthesiology, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Shanghai, 200032, People's Republic of China. drfanghao@163.com.
Jinshan Hospital of Fudan University · CNZhongshan Hospital · CNFudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTelocytes (TCs) are newly identified interstitial cells that participate in tissue protection and repair. The present study investigated the mechanisms underlying the protective effect of TCs in a mouse model of respiratory distress.

methodsThe mouse model of acute respiratory distress syndrome (ARDS) was established by intratracheal instillation of lipopolysaccharide (LPS). After instillation of TCs culture medium, lung injury was assessed, and angiogenesis markers, including CD31 and endothelial nitric oxide synthase (eNOS), were detected by immunofluorescence. Bioinformatics analysis was used to screen significantly differentially expressed microRNAs (miRNAs) in cultured TCs stimulated with LPS, and the regulation of downstream angiogenesis genes by these miRNAs was analysed and verified. PI3K subunits and pathways were evaluated by using a PI3K p110α inhibitor to study the involved mechanisms.

resultsIn ARDS mice, instillation of TCs culture medium ameliorated LPS-induced inflammation and lung injury and increased the protein levels of CD31 and eNOS in the injured lungs. A total of 7 miRNAs and 1899 mRNAs were differentially regulated in TCs stimulated with LPS. Functional prediction analysis showed that the differentially expressed mRNAs were enriched in angiogenesis-related processes, which were highly correlated with miR-21a-3p. Culture medium from TCs with miR-21a-3p inhibition failed to promote angiogenesis in mouse models of LPS-induced ARDS. In cultured TCs, LPS stimulation upregulated the expression of miR-21a-3p, which further targeted the transcription factor E2F8 and decreased Notch2 protein expression. TCs culture medium enhanced hemangioendothelioma endothelial cells (EOMA cells) proliferation, which was blocked by the miR-21a-3p inhibitor. The PI3K p110α inhibitor decreased vascular endothelial growth factor levels in LPS-stimulated TCs and reversed the enhancing effect of TCs culture medium on EOMA cells proliferation.

conclusionsTCs exerted protective effects under inflammatory conditions by promoting angiogenesis via miR-21a-3p. The PI3K p110α subunit and transcriptional factor E2F8 could be involved in this process.

Indexed as

Neovascularization, PhysiologicAnimalsCell LineCell ProliferationDisease Models, AnimalGene Expression ProfilingGene Expression RegulationInflammationLipopolysaccharidesMaleMice, Inbred C57BLMicroRNAsModels, BiologicalPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReproducibility of ResultsLipopolysaccharidesMicroRNAsMIRN21 microRNA, mousePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRNA, MessengerTOR Serine-Threonine KinasesAcute respiratory distress syndromeAngiogenesismiRNA-21a-3pPI3K p110αTelocyte

Identifiers

PMID31878977
PMCPMC6933909
OpenAlexW2996887966

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.