Evidence map›Paper›PMID 39757225›Full record

ArticleStem cell research & therapy2025

hAMSCs regulate EMT in the progression of experimental pulmonary fibrosis through delivering miR-181a-5p targeting TGFBR1.

Yanyang Wang, Chan Liu, Nuoxin Wang, Dong Weng, Yan Zhao, Hongyu Yang, Haoyuan Wang, Shangfu Xu, Jianmei Gao, Changhui Lang and 3 more

Abstract read
In one paragraph

Article in Stem cell research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

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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

13 authors.

Yanyang WangKey Laboratory of Cell Engineering of Guizhou Province, Affiliated Hospital of Zunyi Medical University, Zunyi, 563000, Guizhou, China.
Chan LiuKey Laboratory of Cell Engineering of Guizhou Province, Affiliated Hospital of Zunyi Medical University, Zunyi, 563000, Guizhou, China.
Nuoxin WangKey Laboratory of Cell Engineering of Guizhou Province, Affiliated Hospital of Zunyi Medical University, Zunyi, 563000, Guizhou, China.
Dong WengKey Laboratory of Cell Engineering of Guizhou Province, Affiliated Hospital of Zunyi Medical University, Zunyi, 563000, Guizhou, China.
Yan ZhaoDepartment of Prevention Healthcare, Southwest Hospital, First Affiliated Hospital of the Army Medical University, Chongqing, 400038, China.
Hongyu YangKey Laboratory of Cell Engineering of Guizhou Province, Affiliated Hospital of Zunyi Medical University, Zunyi, 563000, Guizhou, China.
Haoyuan WangDepartment of Cardiothoracic Surgery, Liuzhou People's Hospital, Liuzhou, 545001, Guangxi, China.
Shangfu XuKey Laboratory of Cell Engineering of Guizhou Province, Affiliated Hospital of Zunyi Medical University, Zunyi, 563000, Guizhou, China.
Jianmei GaoKey Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnomedicine of Ministry of Education, Zunyi, 563000, Guizhou, China.
Changhui LangDepartment of Pediatrics, Affiliated Hospital of Zunyi Medical University, Zunyi, 563000, Guizhou, China.
Zhenhai FanKey Laboratory of Cell Engineering of Guizhou Province, Affiliated Hospital of Zunyi Medical University, Zunyi, 563000, Guizhou, China.
Limei YuKey Laboratory of Cell Engineering of Guizhou Province, Affiliated Hospital of Zunyi Medical University, Zunyi, 563000, Guizhou, China.
Zhixu HeCenter of Tissue Engineering and Stem Cell Research, Guizhou Medical University, Guiyang, 550025, Guizhou, China. hzx@gmc.edu.cn.

Funding

Innovative Research Group Project of the National Natural Science Foundation of China No : 32270848Ministry of Scientific and Technological Development, Higher Education and Information Society Grant Number:2020-39Science and Technology Program of Guizhou Province No. QKH-JC-ZK[2023]YB586Science and Technology Program of Guizhou Province Qian Ke He【2020】4Y192
6 · The paper itself

Abstract

backgroundPulmonary fibrosis (PF) is a common and multidimensional devastating interstitial lung disease. The development of novel and more effective interventions for PF is an urgent clinical need. A previous study has found that miR-181a-5p plays an important role in the development of PF, and human amniotic mesenchymal stem cells (hAMSCs) exert potent therapeutic potential on PF. However, whether hAMSCs act on PF by delivering miR-181a-5p and its detailed mechanism still remain unknown. Thus, this study was designed to investigate the underlying possible mechanism of hAMSCs on PF in bleomycin (BLM)-induced mouse PF model, and a co-culture system of hAMSCs and A549 cells epithelial mesenchymal transition (EMT) model, focusing on its effects on collagen deposition, EMT, and epithelial cell cycle regulation.

methodshAMSCs with different miR-181a-5p expression levels were constructed. BLM (4 mg/kg) was used to create a PF model, while TGF-β1 was used to induce A549 cells to construct an EMT model. Furthermore, the effects of different miR-181a-5p expression in hAMSCs on collagen deposition and EMT during lung fibrosis were assessed in vivo and in vitro.

resultsWe found that hAMSCs exerted anti-fibrotic effect in BLM-induced mouse PF model. Moreover, hAMSCs also exerted protective effect on TGFβ1-induced A549 cell EMT model. Furthermore, hAMSCs ameliorated PF by promoting epithelial cell proliferation, reducing epithelial cell apoptosis, and attenuating EMT of epithelial cells through paracrine effects. hAMSCs regulated EMT in PF through delivering miR-181a-5p targeting TGFBR1.

conclusionsOur findings reveal for the first time that hAMSCs inhibit PF by promoting epithelial cell proliferation, reducing epithelial cell apoptosis, and attenuating EMT. Mechanistically, the therapeutic effect of hMASCs on PF is achieved through delivering miR-181a-5p targeting TGFBR1.

Indexed as

Epithelial-Mesenchymal TransitionMesenchymal Stem CellsMicroRNAsPulmonary FibrosisReceptor, Transforming Growth Factor-beta Type IA549 CellsAmnionAnimalsBleomycinDisease Models, AnimalHumansMaleMiceMice, Inbred C57BLTransforming Growth Factor beta1BleomycinMicroRNAsMIrn181 microRNA, humanmirn181 microRNA, mouseReceptor, Transforming Growth Factor-beta Type ITgfbr1 protein, mouseTransforming Growth Factor beta1Amniotic membrane mesenchymal stem cellsEpithelial mesenchymal transitionhAMSCsmiR-181a-5pPulmonary fibrosisTGFBR1

Identifiers

PMID39757225
PMCPMC11702096

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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Registered trials

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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 Socratic graph.