Evidence map›Paper›PMID 34408418›Full record

ArticleInternational journal of nanomedicine2021

Exosomal lncRNA CHL1-AS1 Derived from Peritoneal Macrophages Promotes the Progression of Endometriosis via the miR-610/MDM2 Axis.

Ting Liu, Mei Liu, Caihua Zheng, Daoyan Zhang, Mingbao Li, Lu Zhang

Open access · goldAbstract read
In one paragraph

Article in International journal of nanomedicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 2 pooled it
4.4field-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

21 citing papers in PubMed, 2 syntheses or guidelines pooled it, 34 citations in OpenAlex.

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  15. Applications of nanomaterials in endometriosis treatment.Frontiers in bioengineering and biotechnology · 2023
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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

6 authors at 3 institutions in 1 country.

Ting LiuDepartment of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Jinan, 250012, People's Republic of China.ORCID 0000-0003-4157-4812
Mei LiuDepartment of Obstetrics, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, 250011, People's Republic of China.
Caihua ZhengDepartment of Obstetrics, Changle County Hospital of Traditional Chinese Medicine, Changle, 262400, People's Republic of China.
Daoyan ZhangDepartment of Obstetrics and Gynecology, People's Hospital of Qihe County, Qihe, 251100, People's Republic of China.
Mingbao LiDepartment of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Jinan, 250012, People's Republic of China.
Lu ZhangDepartment of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Jinan, 250012, People's Republic of China.
Qilu Hospital of Shandong University · CNQihe People's Hospital · CNShandong University of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundExosomes secreted by peritoneal macrophages (pMφ) are deeply involved in the development of endometriosis (EMs). Exosomes can mediate cell-to-cell communication by transferring biological molecules. This study aimed to explore the effect and mechanism of exosomal long non-coding RNA (lncRNA) CHL1-AS1 derived from pMφ on EMs. MATERIALS AND

methodsExosomes (exo) from pMφ were isolated, identified, and co-cultured with ectopic endometrial stromal cells (eESCs) to investigate the biological functions of pMφ-exo. qRT-PCR was used to detect the expression of lncRNA CHL1-AS1 in pMφ-exo from EMs and control patients and verify the transportation of lncRNA CHL1-AS1 from pMφ to eESCs. The effects of exosomal lncRNA CHL1-AS1 on eESC proliferation, migration, invasion, and apoptosis were also detected. The relationships among lncRNA CHL1-AS1, miR-610, and MDM2 (mouse double minute 2) were verified by dual-luciferase reporter assay. The in vivo experiments were conducted to verify the effects of exosomal lncRNA on EMs using a xenograft model of EMs.

resultsExosomes from pMφ were successfully isolated. EMs-pMφ-exo promoted eESC proliferation, migration, and invasion and inhibited their apoptosis. lncRNA CHL1-AS1 was upregulated in EMs-pMφ-exo and transported from pMφ to eESCs via exosomes. lncRNA CHL1-AS1 was found to act as a competing endogenous RNA of miR‑610 to promote the expression of MDM2. EMs-pMφ-exo shuttled lncRNA CHL1-AS1 to promote eESC proliferation, migration, and invasion and inhibit apoptosis by downregulating miR-610 and upregulating MDM2. Furthermore, exosomal lncRNA CHL1-AS1 promoted EMs lesions growth by increasing MDM2 in vivo.

conclusionThe results demonstrate that exosomal lncRNA CHL1-AS1 promotes the proliferation, migration, and invasion of eESCs and inhibits their apoptosis by downregulating miR-610 and upregulating MDM2, which might be a potential therapeutic target for EMs.

Indexed as

EndometriosisMicroRNAsRNA, Long NoncodingAnimalsCell MovementCell ProliferationFemaleHumansMacrophages, PeritonealMiceProto-Oncogene Proteins c-mdm2MDM2 protein, humanMicroRNAsMIRN610 microRNA, humanProto-Oncogene Proteins c-mdm2RNA, Long NoncodingendometriosisexosomeslncRNA CHL1-AS1MDM2miR-610peritoneal macrophages

Identifiers

PMID34408418
PMCPMC8367089
OpenAlexW3192261101

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.