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Hsa_circ_0006872 promotes cigarette smoke-induced apoptosis, inflammation and oxidative stress in HPMECs and BEAS-2B cells through the miR-145-5p/NF-κB axis.

Abstract：

:Cigarette smoke is a major cause of chronic obstructive pulmonary disease (COPD). Circular RNAs (circRNAs) are involved in regulating various biological processes. This study aimed to explore the role and molecular basis of hsa_circ_0006872 in cigarette smoke extract (CSE)-induced cell injury. HPMECs and BEAS-2B cells were treated with CSE to mimic COPD in vitro. The levels of hsa_circ_0006872 and miR-145-5p were measured by quantitative real-time polymerase chain reaction. Cell proliferation was assessed via Cell Counting Kit-8 (CCK-8) and colony formation assays. Flow cytometry was used to evaluate apoptosis and cell cycle. The levels of inflammatory factors were assayed via enzyme-linked immunosorbent assay (ELISA). The levels of oxidative stress markers were determined via commercial kits. The interaction between hsa_circ_0006872 and miR-145-5p was confirmed by dual-luciferase reporter assay and RNA immunoprecipitation assay. Protein expression was measured using Western blot assay. Hsa_circ_0006872 level was elevated in COPD patients and was negatively correlated with miR-145-5p level. CSE exposure promoted apoptosis, inflammation and oxidative stress of HPMECs and BEAS-2B cells, while hsa_circ_0006872 down-regulation undermined the effects. In addition, hsa_circ_0006872 silencing inhibited CSE-induced cell injury via regulating miR-145-5p. Moreover, CSE contributed to the activation of NF-κB pathway through hsa_circ_0006872/miR-145-5p axis. Hsa_circ_0006872 facilitated CSE-triggered apoptosis, inflammation and oxidative stress in HPMECs and BEAS-2B cells by regulating miR-145-5p/NF-κB pathway.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Xue M,Peng N,Zhu X,Zhang H

doi

10.1016/j.bbrc.2020.11.044

subject

Has Abstract

pub_date

2021-01-01 00:00:00

pages

553-560

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(20)32086-6

journal_volume

534

pub_type

杂志文章

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