miR-33 and RIP140 participate in LPS-induced acute lung injury

Abstract

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 theinflammatory response in macrophages. In this study, we sought to investigate whether miR-33 and RIP140 participate in ALI inducedby LPS.Materials and methods: First, we isolated and identified PMVECs from BALB/c mice. Subsequently, both PMVECs and BALB/c micewere 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 levelswere 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-33expression 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, whichmay help uncover the mechanism of ALI.