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 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 methodsFirst, 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.ResultsOur 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).ConclusionThis 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.
Highlights
Acute lung injury (ALI) is a critical clinical disease caused by uncontrolled inflammation [1]
Our results demonstrated that LPS can induce pulmonary microvascular endothelial cells (PMVECs) injury and ALI and that LPS treatment significantly decreased miR-33 expression compared with controls (P < 0.001, n = 5)
This study is the first to confirm that both miR-33 and Receptor-interacting protein 140 (RIP140) participate in LPS-induced PMVEC injury and ALI, which may help uncover the mechanism of ALI
Summary
Acute lung injury (ALI) is a critical clinical disease caused by uncontrolled inflammation [1]. Overexpression of inflammatory mediators as a result of a variety of factors excluding cardiogenic factors can lead to ALI, and sepsis represents one of the major factors [2]. Lipopolysaccharide (LPS) is the main component of the outer membrane of gram-negative bacteria, which are a major pathogenic cause of sepsis [3]. LPS can attack pulmonary microvascular endothelial cells (PMVECs), resulting in leakage of protein-rich edema fluid as a result of PMVEC injury and barrier dysfunction. The main pathologic feature of ALI is pulmonary edema due to the increase in PMVEC permeability [4,5]. PMVEC function is receiving increasing attention in ALI research
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