LAUSR

The role of microRNAs has been recently identified in chronic obstructive pulmonary disease (COPD). This study aimed to examine the role of miR-132 in the pathophysiology of COPD and to explore the underlying molecular mechanisms of miR-132 in COPD. MiR-132 and suppressor of cytokine signaling 5 (SOCS5) mRNA expression were detected by qRT-PCR. The number of CD4+ and CD8+ T cells was analyzed by flow cytometry. SOCS5 and epidermal growth factor receptor (EGFR) protein levels were determined by western blot. Interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) concentrations were measured by ELISA. MiR-132 expression was up-regulated in the serum from COPD patients and smokers compared with nonsmoker controls. The number of CD8+ T cells was significantly increased in the serum from COPD patients and smokers. MiR-132 expression was negatively correlated with FEV1/FVC%, and positively correlated with CD8+ T cells (%). MiR-132 overexpression repressed SOCS5 expression via directly targeting SOCS5 3'UTR in human monocyte-like cells (THP-1), which was confirmed by luciferase reporter assay. MiR-132 overexpression increased EGFR protein levels and the concentrations of inflammatory cytokines (IL-1β and TNF-α) in THP-1 cells, and these effects were attenuated by enforced expression of SOCS5. Further, cigarette smoke extract (CSE) treatment up-regulated miR-132 expression, down-regulated SOCS5 expression, and increased inflammatory cytokines levels, which was attenuated by miR-132 knockdown in THP-1 cells. Consistent findings were also found in the human bronchial epithelial cells (BEAS-2B). Collectively, our data implicated that miR-132 may promote inflammation in THP-1 and BEAS-2B cells at least via targeting SOCS5 in COPD.