miR-33 和 RIP140 参与 LPS 诱导的急性肺损伤。
miR-33 and RIP140 participate in LPS-induced acute lung injury.
出版信息
Turk J Med Sci. 2019 Feb 11;49(1):422-428. doi: 10.3906/sag-1804-173.
BACKGROUND/AIM: Pulmonary microvascular endothelial cells (PMVECs) play a pivotal role in the process of acute lung injury (ALI), which can be induced by lipopolysaccharide (LPS). Numerous reports have indicated that both miR-33 and RIP140 are involved in the inflammatory response in macrophages. In this study, we sought to investigate whether miR-33 and RIP140 participate in ALI induced by LPS.
MATERIALS AND METHODS
First, we isolated and identified PMVECs from BALB/c mice. Subsequently, both PMVECs and BALB/c mice were treated with PBS, LPS, or pyrrolidine dithiocarbamate (PDTC) plus LPS and divided into three groups: control (PBS), LPS (LPS), and L+P (LPS plus PDTC) groups. We assessed pathology by hematoxylin and eosin staining, and miR-33 and RIP140 expression levels were examined using quantitative PCR and Western blot analyses.
RESULTS
Our results demonstrated that LPS can induce PMVEC injury and ALI and that LPS treatment significantly decreased miR-33 expression compared with controls (P < 0.001, n = 5). On the contrary, RIP140 was markedly overexpressed by LPS treatment (P < 0.001, n = 5). However, this alteration can be inhibited by pretreatment with PDTC before LPS (P < 0.05, n = 5).
CONCLUSION
This study is the first to confirm that both miR-33 and RIP140 participate in LPS-induced PMVEC injury and ALI, which may help uncover the mechanism of ALI
背景/目的：肺微血管内皮细胞（PMVECs）在急性肺损伤（ALI）过程中发挥关键作用，脂多糖（LPS）可诱导 ALI。许多报道表明，miR-33 和 RIP140 均参与巨噬细胞中的炎症反应。在本研究中，我们旨在探讨 miR-33 和 RIP140 是否参与 LPS 诱导的 ALI。
材料和方法
首先，我们从 BALB/c 小鼠中分离和鉴定 PMVECs。随后，用 PBS、LPS 或吡咯烷二硫代氨基甲酸盐（PDTC）+LPS 处理 PMVECs 和 BALB/c 小鼠，并将其分为三组：对照组（PBS）、LPS 组（LPS）和 L+P 组（LPS+PDTC）。通过苏木精和伊红染色评估病理学，并用定量 PCR 和 Western blot 分析检测 miR-33 和 RIP140 的表达水平。
结果
我们的结果表明，LPS 可诱导 PMVEC 损伤和 ALI，并且与对照组相比，LPS 处理可显著降低 miR-33 的表达（P<0.001，n=5）。相反，LPS 处理使 RIP140 明显过表达（P<0.001，n=5）。但是，用 LPS 预处理前用 PDTC 处理可抑制这种改变（P<0.05，n=5）。
结论
本研究首次证实，miR-33 和 RIP140 均参与 LPS 诱导的 PMVEC 损伤和 ALI，这可能有助于揭示 ALI 的机制。
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