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J. Hazard. Mater., 2022 Nov 24;445:130466 | https://doi.org/10.1016/j.jhazmat.2022.130466 Specific upregulation of extracellular miR-6238 in particulate matter-induced acute lung injury and its immunomodulation

Sujeong Park^a, Miji Kim^a, Minkyung Park^b,c, Yang Jin^d, Seon-Jin Lee^b,c,1, Heedoo Lee^a,1

^aDepartment of Biology and Chemistry, Changwon National University, Changwon 51140, South Korea
^bDepartment of Functional Genomics, University of Science and Technology (UST), Daejeon 34113, South Korea
^cEnvironmental Disease Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon 34141, South Korea
^dDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Boston University School of Medicine, Boston, MA 02118, USA

¹These authors contributed equally to this work.
Corresponding authors: Seon-Jin Lee, Heedoo Lee

Abstract

Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are life-threatening diseases characterized by a severe inflammatory response and the destruction of alveolar epithelium and endothelium. ALI/ARDS is caused by pathogens and toxic environmental stimuli, such as particulate matter (PM). However, the general symptoms of ALI/ARDS are similar, and determining the cause of lung injury is often challenging. In this study, we investigated whether there is a critical miRNA that characterizes PM-induced ALI. We found that the expression of miR-6238 is specifically upregulated in lung tissue and lung-derived extracellular vesicles (EVs) in response to PM exposure. Notably, bacterial endotoxin (Lipopolysaccharide; LPS or peptidoglycan; PTG) does not induce the expression of miR-6238 in the lung. Instead, the expression of miR-155 is dramatically increased in LPS-induced ALI. We further demonstrated that human lung epithelial cells and macrophages predominantly produce miR-6238 and miR-155, respectively. Mechanistically, EV-miR-6238 is effectively internalized into alveolar macrophages (AMs) and regulates inflammatory responses in vivo. CXCL3 is a main target of miR-6238 in AMs and modulates neutrophil infiltration into the lung alveoli. Collectively, our findings suggest that miR-6238 is a novel regulator of pulmonary inflammation and a putative biomarker that distinguishes PM-induced ALI from endotoxin (LPS/PTG)-mediated ALI.

논문정보

형식Research article
게재일2022년 11월 (BRIC 등록일 2023-01-11)
연구진국내(교신)+국외 연구진
분야 생명과학 > 생리학

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