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The inhibitor miR-21 regulates macrophage polarization in an experimental model of chronic obstructive pulmonary disease.
Tobacco Induced Diseases ( IF 2.2 ) Pub Date : 2021-09-02 , DOI: 10.18332/tid/140095
JunJuan Lu 1 , LiHua Xie 1 , ShengHua Sun 1
Affiliation  

INTRODUCTION 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. The molecular mechanism of this process is unclear, and it has not been fully elucidated in COPD. METHODS We 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. RESULTS The 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. CONCLUSIONS We 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.

中文翻译:

抑制剂 miR-21 在慢性阻塞性肺疾病的实验模型中调节巨噬细胞极化。

引言 在慢性阻塞性肺疾病 (COPD) 中,巨噬细胞起着不可或缺的作用。在 COPD 患者和吸烟者的肺组织中,可以观察到巨噬细胞向 M2 表型极化。这一过程的分子机制尚不清楚,在 COPD 中尚未完全阐明。方法 我们从杰克逊实验室购买了实验动物 [C57BL/6 和 miR-21-/- C57BL/6(F1)]。通过香烟烟雾(CS)暴露联合腹腔注射香烟烟雾提取物(CSE)建立COPD小鼠模型。RT-PCR 检测炎症因子和 M1 和 M2 巨噬细胞相关标志物的表达水平。通过免疫组织化学染色检测M2巨噬细胞与M1巨噬细胞的比例。结果 RAW264中miR-21水平升高。CSE 干预的 7 个细胞以及 COPD 小鼠的肺组织和骨髓来源的巨噬细胞 (BMDM)。随着时间的推移,CSE 可以逐渐增加 miR-21 的水平。M2巨噬细胞与M1巨噬细胞的比例与miR-21呈正相关。敲低 miR-21 可以减少肺组织损伤。CSE 还增加了与 M2 巨噬细胞相关的相关炎症因子和标志物的水平,而 miR-21 抑制剂可以逆转这种转化。结论 我们证实 CSE 可导致巨噬细胞转化为 M2 表型并增加 miR-21 的表达水平。敲低 miR-21 基因可以抑制巨噬细胞向 COPD 中 M2 表型的转化。M2巨噬细胞与M1巨噬细胞的比例与miR-21呈正相关。敲低 miR-21 可以减少肺组织损伤。CSE 还增加了与 M2 巨噬细胞相关的相关炎症因子和标志物的水平,而 miR-21 抑制剂可以逆转这种转化。结论 我们证实 CSE 可导致巨噬细胞转化为 M2 表型并增加 miR-21 的表达水平。敲低 miR-21 基因可以抑制巨噬细胞向 COPD 中 M2 表型的转化。M2巨噬细胞与M1巨噬细胞的比例与miR-21呈正相关。敲低 miR-21 可以减少肺组织损伤。CSE 还增加了与 M2 巨噬细胞相关的相关炎症因子和标志物的水平,而 miR-21 抑制剂可以逆转这种转化。结论 我们证实 CSE 可导致巨噬细胞转化为 M2 表型并增加 miR-21 的表达水平。敲低 miR-21 基因可以抑制巨噬细胞向 COPD 中 M2 表型的转化。结论 我们证实 CSE 可导致巨噬细胞转化为 M2 表型并增加 miR-21 的表达水平。敲低 miR-21 基因可以抑制巨噬细胞向 COPD 中 M2 表型的转化。结论 我们证实 CSE 可导致巨噬细胞转化为 M2 表型并增加 miR-21 的表达水平。敲低 miR-21 基因可以抑制巨噬细胞向 COPD 中 M2 表型的转化。
更新日期:2021-09-02
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