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<p>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.</p>

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

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年2月10日

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

摘要

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.