Open AccessAnalysis the effect of miR ‐141‐3p/ HMGB1 in LPS ‐induced mucus production and the apoptosis in nasal epithelial cells
Author(s) -
Zhu YongMing,
Wu Feng,
Zhou JieYu
Publication year - 2020
Publication title -
the kaohsiung journal of medical sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.439
H-Index - 36
eISSN - 2410-8650
pISSN - 1607-551X
DOI - 10.1002/kjm2.12215
Subject(s) - lipopolysaccharide , medicine , hmgb1 , apoptosis , downregulation and upregulation , mucin , microrna , mucus , immunology , cancer research , pathology , inflammation , biology , gene , biochemistry , ecology
Abstract Allergic rhinitis (AR) is an allergic disease characterized by immunoglobulin E (IgE)‐mediated type I hypersensitivity disorder. In the current study, we illuminated the potential roles of microRNA‐141‐3p (miR‐141‐3p) in lipopolysaccharide (LPS)‐induced mucus production and the apoptosis in nasal epithelial cells (NECs). We demonstrated that miR‐141‐3p was significantly downregulated in nasal tissues from patients with AR and LPS‐treated NECs. Upregulation of miR‐141‐3p decreased the level of mucin 5AC (MUC5AC) in LPS‐treated NECs and induced NECs apoptosis. High Mobility Group Box 1 (HMGB1) was proved as a target of miR‐141‐3p and miR‐141‐3p negatively regulated its expression. In addition, we observed that HMGB1 was overexpressed in nasal mucosal tissues from patients with AR and LPS‐treated NECs. Finally, we proved that miR‐141‐3p decreased the level of MUAC5AC in LPS‐treated NECs through regulating HMGB1. In conclusion, miR‐141‐3p inhibited LPS‐induced MUAC5AC production and the apoptosis of LPS‐treated NECs by targeting HMGB1.