MiR-548ar-3p increases cigarette smoke extract-induced chronic obstructive pulmonary disease (COPD) injury through solute carrier family 17 member 9 (SLC17A9)


  • Longju Zhang Department of Respiratory and Critical Care Medicine, The Third Affiliated Hospital of Zunyi Medical University (The First People's Hospital of Zunyi), Zunyi 563000, Guizhou, PR China https://orcid.org/0000-0003-1976-1558
  • Xiaoli Liu Department of Respiratory and Critical Care Medicine, Affiliated Hospital of Zunyi Medical University, Zunyi 563000, Guizhou, PR China https://orcid.org/0000-0001-6798-7055
  • Yi Zheng Department of Physiology, Zunyi Medical And Pharmaceutical College, Zunyi 563006, Guizhou, PR China https://orcid.org/0000-0002-7825-5594
  • Fei Du Department of Respiratory and Critical Care Medicine, The Third Affiliated Hospital of Zunyi Medical University (The First People's Hospital of Zunyi), Zunyi 563000, Guizhou, PR China https://orcid.org/0000-0002-0354-1131
  • Gang He Department of Respiratory and Critical Care Medicine, The Third Affiliated Hospital of Zunyi Medical University (The First People's Hospital of Zunyi), Zunyi 563000, Guizhou, PR China https://orcid.org/0000-0002-3748-2213




chronic obstructive pulmonary disease (COPD), cigarette smoke extract (CSE), miR-548ar-3p, solute carrier family 17 member 9 (SLC17A9), high-throughput sequencing, human bronchial epithelial cells


Paper description:

  • The pathogenesis of chronic obstructive pulmonary disease (COPD) caused by smoking is unclear.
  • miR-548ar-3p was selected by high-throughput sequencing of peripheral blood from smoking (COPD) and non-smoking (normal) individuals. A miR-548ar-3p mimic was transfected into human bronchial epithelial (HBE) cells and a COPD model was established by treating HBE cells with cigarette smoke extract (CSE). The effect of miR-548ar-3p on cell proliferation, apoptosis and SLC17A9 protein expression was examined.
  • miR-548ar-3p was expressed at a lower level in COPD patients. It caused decreased cell viablity, promoted apoptosis and increased SLC17A9 protein expression.
  • miR-548ar-3p may aggravate CSE-induced COPD injury through SLC17A9.

Abstract: This study investigated the effect of microRNA mir-548ar-3p on cigarette smoke extract (CSE)-induced chronic obstructive pulmonary disease (COPD). High-throughput sequencing was performed on peripheral blood from smoking COPD patients and non-smoking individuals with normal pulmonary function, and miR-548ar-3p RNA, possessing large differential expression was selected. Experimental groups were divided into control, experimental model (EM), EM+mimic miRNA, negative control (NC) and EM+miR-548ar-3p groups; an empty vector or miR-548ar-3p mimic was transfected into human bronchial epithelial (HBE) cells. A COPD model was established by treating HBE cells with CSE. Cell viability, apoptosis and solute carrier family 17 member 9 (SLC17A9) protein expression were examined by cell counting kit-8, flow cytometry and Western blotting, respectively. Cell viability in the EM+miR-548ar-3p group decreased significantly, and the apoptosis rate and SLC17A9 protein expression increased significantly compared with the control (P<0.05, all groups). In smoking COPD patients, interferon (IFN)-γ and interleukin (IL)-17α expression detected by ELISA was significantly higher than in normal individuals. miR-548ar-3p expression was significantly lower (P<0.05, all groups). These findings suggest that miR-548ar-3p was expressed at a lower level in COPD patients. miR-548ar-3p may increase the extent of CSE-induced COPD injury through SLC17A9


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How to Cite

Zhang L, Liu X, Zheng Y, Du F, He G. MiR-548ar-3p increases cigarette smoke extract-induced chronic obstructive pulmonary disease (COPD) injury through solute carrier family 17 member 9 (SLC17A9). Arch Biol Sci [Internet]. 2022Apr.1 [cited 2024Jul.20];74(1):97-105. Available from: https://www.serbiosoc.org.rs/arch/index.php/abs/article/view/7465