RESUMO
Glucagon-like peptide-1 (GLP1) is an important insulin secretagogue that possesses antiinflammatory effects. GLP1 receptor (GLP1R) agonists have been demonstrated to serve a pivotal role in the treatment of obstructive lung diseases, including chronic obstructive pulmonary disease (COPD). However, the specific function and underlying mechanisms of GLP1R in COPD remain uncertain. The aim of the present study was to investigate the action and underlying mechanisms of GLP1R in airway smooth muscle (ASM) cells from COPD patients. GLP1R expression levels were markedly decreased in ASM cells from COPD patients compared with those from healthy controls. ASM cell proliferation and migration, and the levels of the inflammatory cytokines interleukin (IL)1ß, IL4, tumor necrosis factor (TNF)α, and granulocytemacrophage colonystimulating factor (GMCSF) were measured. Transfection of pcDNA3.1GLP1R had inhibitory effects on ASM cell proliferation and migration, whereas GLP1R small interfering (si)RNA reversed these effects. Furthermore, the present study demonstrated that GLP1R overexpression markedly suppressed IL1ß, IL4, TNFα and GMCSF levels. GLP1R overexpression upregulated the expression levels of adenosine triphosphatebinding cassette, subfamily A, member 1 (ABCA1) in ASM cells, and the effects of GLP1R on cell proliferation and migration, and inflammatory cytokine expression in ASM cells was abolished by siRNAmediated silencing of ABCA1. The results of the present study suggested that GLP1R contributes to COPD pathology, potentially via an ABCA1mediated pathway.