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Published on: April 10, 2019
Bone Marrow Mesenchymal Stem Cells-Derived Exosomes Inhibit Apoptosis of Pulmonary Microvascular Endothelial Cells in
Qing Song1,2,3,4, Aiyuan Zhou5, Wei Cheng1,2,3,4
1Department of Respiratory and Critical Care Medicine, the Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, People's Republic of China.
Background:
Bone marrow mesenchymal stem cells (BMSCs)-derived exosomes are rich in a variety of active substances, including microRNA (miR) and have shown powerful therapeutic effects to ameliorate cell injury and diseases. However, the role of BMSCs-derived exosomes on chronic obstructive pulmonary disease (COPD) has been poorly studied. In addition, pulmonary microvascular endothelial cells (PMVECs) apoptosis contributes to the onset of COPD. Inhibition of PMVECs apoptosis can reverse COPD changes. Therefore, the aim of this study was to explore the role of BMSCs-derived exosomes in the apoptosis of PMVECs in COPD and to investigate the potential mechanisms.
Methods:
We isolated and characterized normal mouse BMSCs-derived exosomes and PMVECs. We performed miR sequencing of BMSCs-derived exosomes. We transfected PMVECs with the miR-30b mimic and Wnt5a overexpression plasmid to assess the underlying mechanisms. Cigarette smoke extract (CSE)-induced COPD mice were treated with exosomes and HBLV-mmu-miR-30b via intratracheal instillation. Finally, we determined the expression of miR-30b and Wnt5a in tissues from patients with COPD.
Results:
BMSCs-derived exosomes could significantly reduce apoptosis of CSE-induced PMVECs and increase the expression of miR-30b (p<0.05). Based on miR sequencing, miR-30b was highly enriched in BMSCs-derived exosomes. The knockdown of miR-30b in BMSCs-derived exosomes could increase the apoptosis of CSE-induced PMVECs (p<0.05). miR-30b overexpression significantly reduced apoptosis and repressed Wnt5a protein expression in CSE-induced PMVECs (p<0.05). Furthermore, Wnt5a overexpression reversed the anti-apoptotic effect of miR-30b on CSE-induced PMVECs (p<0.05). In addition, compared with the COPD group, treatment with BMSCs-derived exosomes and miR-30b overexpression could alleviate emphysema changes, decrease the mean linear intercept and alveolar destructive index, reduce apoptosis, increase the expression of miR-30b, and decrease the expression of Wnt5a in lung tissue (p<0.05). Finally, miR-30b expression was decreased in patients with COPD, while Wnt5a expression was increased in these patients (p<0.05).
Conclusion:
BMSCs-derived exosomes could improve the damage of COPD perhaps by delivering miR-30b. miR-30b could reduce apoptosis of CSE-induced PMVECs by targeting Wnt5a.
