Abstract
INTRODUCTIONIn chronic obstructive pulmonary disease (COPD), macrophages play an indispensable role. In the lung tissues of COPD patients and smokers, macrophages can be observed to polarize towards M2 phenotype. The molecular mechanism of this process is unclear, and it has not been fully elucidated in COPD.METHODSWe bought laboratory animals [C57BL/6 and miR-21–/– C57BL/6(F1)] from the Jackson Laboratory. The model of COPD mice was established by cigarette smoke (CS) exposure combined with intraperitoneal injection of cigarette smoke extract (CSE). RT-PCR detected the expression levels of inflammatory factors and markers associated with M1 and M2 macrophages. The ratio of M2 macrophages to M1 macrophages was detected by immunohistochemical staining.RESULTSThe level of miR-21 was increased in RAW264.7 cells intervened by CSE and in lung tissue and bone marrow-derived macrophages (BMDMs) from COPD mice. CSE can gradually over time increase the level of miR-21. The proportion of M2 macrophages to M1 macrophages had a positive correlation with miR-21. Knockdowning miR-21 can reduce lung tissue damage. CSE also increased the levels of related inflammatory factors and markers associated with M2 macrophages, and an miR-21 inhibitor can reverse this conversion.CONCLUSIONSWe confirmed that CSE can lead to macrophage transformation to the M2 phenotype and an increase in the expression level of miR-21. Knockdown of the miR-21 gene could inhibit the transformation of macrophages to the M2 phenotype in COPD.
Highlights
In chronic obstructive pulmonary disease (COPD), macrophages play an indispensable role
The expression of miR-21 is up-regulated in RAW264.7 cells intervened by cigarette smoke extract (CSE) and lung tissue and bone marrow-derived macrophages (BMDMs) from COPD mouse model
Our experiment detected the expression of miR21 in RAW264.7 cells intervened by CSE and lung tissue and BMDMs from COPD mouse model and miR-21-/- mice using RT-PCR
Summary
In chronic obstructive pulmonary disease (COPD), macrophages play an indispensable role. In the lung tissues of COPD patients and smokers, macrophages can be observed to polarize towards M2 phenotype. Multiple studies have shown that the number of macrophages in the lung tissue of COPD patients is increased; in addition, there is a correlation between disease progression and the number of macrophages[5,6]. Alveolar macrophages (AM) play an indispensable role in the occurrence and development of COPD, and, at the same time, it can affect the structure of lung tissue through the initiation and degeneration of inflammation[7]. Since a large number of M1-type macrophage-related cytokines, such as TNF-α and IL-8, are found in bronchoalveolar lavage fluid (BAL), pulmonary macrophages from patients with COPD have been recommended to display M1 phenotypes[9]. The regulatory mechanism of macrophage polarization in COPD is unclear
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