Evidence map›Paper›PMID 34743197›Full record

ArticleCell death & disease2021

Functional delivery of lncRNA TUG1 by endothelial progenitor cells derived extracellular vesicles confers anti-inflammatory macrophage polarization in sepsis via impairing miR-9-5p-targeted SIRT1 inhibition.

Wentao Ma, Weihong Zhang, Bing Cui, Jing Gao, Qiuhong Liu, Mengying Yao, Hanbing Ning, Lihua Xing

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 5% 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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.

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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

8 authors at 3 institutions in 1 country.

Wentao Ma *Department of Respiratory Intensive Care Unit, First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, P.R. China.
Weihong Zhang *Department of Anatomy, School of Nursing and Health College, Zhengzhou University, Zhengzhou, 450001, P.R. China.
Bing CuiDepartment of Nephrology, First Affiliated Hospital, Henan University of Traditional Chinese Medicine, Zhengzhou, 450052, P.R. China.
Jing GaoDepartment of Respiratory Intensive Care Unit, First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, P.R. China.
Qiuhong LiuDepartment of Respiratory Intensive Care Unit, First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, P.R. China.
Mengying YaoDepartment of Respiratory Intensive Care Unit, First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, P.R. China. xxMYYao@163.com.ORCID 0000-0002-4203-1599
Hanbing NingDepartment of Digestive Diseases, First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, P.R. China. nhbing419@qq.com.
Lihua XingDepartment of Respiratory Intensive Care Unit, First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, P.R. China. cexdzcxotbxvr@163.com.
First Affiliated Hospital of Zhengzhou University · CNFirst Affiliated Hospital of Henan University of Traditional Chinese Medicine · CNZhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The delivery of biomolecules by extracellular vesicles (EVs) derived from endothelial progenitor cells (EPCs) has been proven to ameliorate sepsis, yet the therapeutic mechanism remains to be elucidated. Taurine upregulated gene 1 (TUG1) is a long noncoding RNA (lncRNA) that is downregulated in sepsis. The current study was designed to explore the role of EPCs derived EVs transmitting TUG1 in macrophage polarization and macrophage-mediated inflammation in a cecal ligation and puncture (CLP)-induced sepsis mouse model. TUG1 was underexpressed in CLP-induced sepsis, and its reexpression induced anti-inflammatory macrophage polarization and suppressed macrophage-medicated inflammatory injury to the pulmonary vascular endothelium. EPCs derived EVs transmitted TUG1 to promote M2 macrophage polarization. Luciferase, RIP, and RNA pull-down assays showed that TUG1 could competitively bind to microRNA-9-5p (miR-9-5p) to upregulate the expression of sirtuin 1 (SIRT1). Furthermore, EPCs derived EVs transmitted TUG1 to promote M2 macrophage polarization through the impairment of miR-9-5p-dependent SIRT1 inhibition. Finally, EPCs derived EVs carrying TUG1 were verified to ameliorate sepsis-induced organ damage in the murine model. In summary, EPCs derived EVs transmit TUG1 to attenuate sepsis via macrophage M2 polarization. This study also highlights the proinflammatory mechanism associated with miR-9-5p-mediated inhibition of SIRT1, which contributes to a more comprehensive understanding of the pathogenesis of sepsis.

Indexed as

Cell PolarityAnimalsAnti-Inflammatory AgentsBase SequenceDisease Models, AnimalEndothelial Progenitor CellsExtracellular VesiclesInflammationLungMacrophagesMaleMiceMice, Inbred C57BLMicroRNAsModels, BiologicalParticle SizeAnti-Inflammatory Agentslong non-coding RNA TUG1, mouseMicroRNAsMIRN9 microRNA, mouseRNA, Long NoncodingSirt1 protein, mouseSirtuin 1

Identifiers

PMID34743197
PMCPMC8572288
OpenAlexW3212594985

What OpenQuestion holds

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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.