MiR‐342 attenuates lipopolysaccharide‐induced acute lung injury via inhibiting MAPK1 expression

Micro RNA (miRNA) and mitogen‐activated protein kinase (MAPK) are reported as the crucial regulators of inflammatory responses in acute lung injury (ALI). This study will explore the role of the miR‐342/MAPK1 axis in regulation of lipopolysaccharide (LPS)‐induced ALI. We found that miR‐342 was down‐...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Clinical and experimental pharmacology & physiology 2020-08, Vol.47 (8), p.1448-1454
Hauptverfasser: Zhu, Siliang, Song, Wenke, Sun, Yanqi, Zhou, Yongqin, Kong, Fanpo
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:Micro RNA (miRNA) and mitogen‐activated protein kinase (MAPK) are reported as the crucial regulators of inflammatory responses in acute lung injury (ALI). This study will explore the role of the miR‐342/MAPK1 axis in regulation of lipopolysaccharide (LPS)‐induced ALI. We found that miR‐342 was down‐regulated in LPS‐induced A549 cells compared with the control group with DMSO, accompanied by elevated inflammatory cytokines and apoptosis. Over‐expression of miR‐342 reduced LPS‐induced inflammatory responses and apoptosis in LPS‐stimulated A549 cells, and had a protective role in LPS‐treated mice with ALI by decreasing levels of inflammatory cytokines, improving survival of mice with ALI, and ameliorating the lung permeability. Dual‐luciferase reporter gene assay demonstrated that miR‐342 regulated the expression of MAPK1 by directly targeting its 3′ untranslated region (3′‐UTR). Mechanistically, MAPK1 silencing abrogated LPS‐induced inflammatory injury in A549 cells, and partially enhanced the protective effect of miR‐342. Therefore, miR‐342 attenuates LPS‐induced ALI by targeting MAPK1 expression, thereby protecting against A549 cell injury induced by LPS and lung injury of mice with ALI.
ISSN:0305-1870
1440-1681
1440-1681
DOI:10.1111/1440-1681.13315