BMSCs exosomes regulate pulmonary microvascular endothelial apoptosis via circRNA_43350/miR-342-5p in COPD.

Yuqin Zeng, Qing Song, Liying Yang, Wei Cheng, Cong Liu, Ling Lin, Shan Cai, Ping Chen

Abstract read

In one paragraph

Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

Authors and funding

8 authors.

Yuqin ZengDepartment of Pulmonary and Critical Care Medicine, The Second Xiangya Hospital, Central South University, Changsha, 410011, China.

Qing SongDepartment of Pulmonary and Critical Care Medicine, The Second Xiangya Hospital, Central South University, Changsha, 410011, China.

Liying YangDepartment of Critical-Care Medicine, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, 250021, China.

Wei ChengDepartment of Pulmonary and Critical Care Medicine, The Second Xiangya Hospital, Central South University, Changsha, 410011, China.

Cong LiuDepartment of Pulmonary and Critical Care Medicine, The Second Xiangya Hospital, Central South University, Changsha, 410011, China.

Ling LinDepartment of Pulmonary and Critical Care Medicine, The Second Xiangya Hospital, Central South University, Changsha, 410011, China.

Shan CaiDepartment of Pulmonary and Critical Care Medicine, The Second Xiangya Hospital, Central South University, Changsha, 410011, China.

Ping ChenDepartment of Pulmonary and Critical Care Medicine, The Second Xiangya Hospital, Central South University, Changsha, 410011, China. pingchen0731@csu.edu.cn.

Funding

National Natural Science Foundation of China 81770046Natural Science Foundation of Hunan Province 2024JJ6561Xiangya Mingyi grant 2013

6 · The paper itself

Abstract

This study was to explore how exosomal circRNA_43350 secreted by bone marrow MSCs (BMSCs) influences the development of chronic obstructive pulmonary disease (COPD). Pulmonary microvascular endothelial cells (PMVECs) and animal models of COPD were constructed in this study. Lung tissue morphometry was observed by hematoxylin and eosin staining. Apoptosis related indicators were measured by flow cytometry, western blot assay and TUNEL staining. The expression of circRNA_43350 and miR-342-5p was analyzed by real-time quantitative polymerase chain reaction. Dual luciferase reporter gene assay was used to investigate the relationship between circRNA_43350 and miR-342-5p. After intervention with BMSCs exosomes from normal mice, the cell apoptosis of PMVECs induced by CSE and emphysema in COPD mice were alleviated. Mmu_circRNA_43350 was highly expressed in normal BMSCs exosomes, while decreased significantly in BMSCs exosomes of COPD. After overexpression of circRNA_43350 in the CSE-induced PMVECs and COPD mice, the apoptosis-related indicators were decreased and the changes of emphysema were alleviated. Additionally, circRNA_43350 acted as a miRNA-342-5p sponge in PMVECs. Further study, we found that circRNA_43350 attenuated CSE-induced apoptosis in PMVECs by regulating the expression of miRNA-342-5p, and overexpression of miRNA-342-5p partially reversed the apoptosis-inhibiting effect of circRNA_43350. CircRNA_43350 derived from BMSCs exosomes attenuated CSE-induced apoptosis in PMVECs by regulating the expression of miRNA-342-5p.

Indexed as

ApoptosisEndothelial CellsExosomesMesenchymal Stem CellsMicroRNAsPulmonary Disease, Chronic ObstructiveRNA, CircularAnimalsDisease Models, AnimalLungMaleMiceMice, Inbred C57BLMicroRNAsRNA, CircularBMSCcircRNA_43350COPDExosomesmiRNA-342-5p

Identifiers

PMID41667834

DOI10.1038/s41598-026-39678-y

PMCPMC12963480

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LicenceCC BY-NC-ND

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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 OpenQuestion graph.