| Summary: | Introduction
Abnormal apoptosis of pulmonary microvascular endothelial cells
(PMVECs) participates in the pathogenesis of COPD. Studies have shown that
microRNAs (miRNAs) contribute to the pathogenesis of pulmonary diseases by
regulating cell apoptosis. The present study aimed to investigate the effects of
miR-216a in cigarette smoke extract (CSE)-induced apoptosis of PMVECs in
COPD and explore the potential mechanisms.
Methods
The emphysema model mice were treated with CSE and CS exposure. The
expression of miR-216a and DNA methyltransferase 1 (DNMT1) was assessed in
emphysema mice and COPD patients. The miR-216a mimic and Lenti-DNMT1
were transfected into PMVECs to identify the underlying mechanisms. The
expression levels of miR-216a and DNMT1 were detected by real-time quantitative
polymerase chain reaction (RT-qPCR) or Western blot. Moreover, cell apoptosis
was examined by flow cytometry assays.
Results
The results show that the expression of miR-216a was decreased, whereas
the expression of DNMT1 was increased in the lung tissue of emphysema mice and
COPD patients. In addition, the expression of miR-216a was significantly reduced
in CSE-treated PMVECs, and the overexpression of miR-216a attenuated CSEinduced
PMVEC apoptosis. Furthermore, the expression of DNMT1 was increased
in the CSE-induced PMVECs and then was reduced after the overexpression of
miR-216a in the CSE-stimulated PMVECs. Luciferase reporter assays confirmed
the target reaction between miR-216a and DNMT1. Also, the overexpression of
DNMT1 was able to reverse the anti-apoptotic effect of miR-216a in CSE-induced
PMVECs.
Conclusions
The results indicate that miR-216a may play a crucial role in CSEinduced
apoptosis by directly regulating its target gene DNMT1 in COPD. It
provides insights into the function of MiR-216a/DNMT1 as a potential molecule
in COPD.
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