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Role of p62/SQSTM1 in lipopolysaccharide (LPS)-induced mucus hypersecretion in bronchial epithelial cells.

Abstract：

AIMS:The aims of this study were to evaluate the effects of p62/SQSTM1 expression levels on lipopolysaccharide (LPS)-induced mucus secretion in BEAS-2B bronchial epithelial cells by measuring expression levels of the MUC5AC gene and the Mucin-5AC (MUC5AC) protein. MATERIALS AND METHODS:Bronchial epithelial cells, BEAS-2B, were treated with LPS at different time points. Rapamycin, an autophagy agonist, was added to the BEAS-2B cells 30 min before LPS treatment. Lentivirus transfection was then used to knock down the expression of p62/SQSTM1 (Sequestosome 1) to investigate changes in the downstream signaling pathway. Western blotting and immunofluorescence were used to study the expression levels of MUC5AC, and reverse transcription-polymerase chain reaction (RT-PCR) was used to study the expression of MUC5AC mRNA. KEY FINDINGS:LPS treatment of BEAS-2B cells inhibited autophagy, activated the nuclear factor kappa B (NF-κB) signaling pathway and increased the expression of MUC5AC. The autophagy agonist, rapamycin, activated autophagy, inhibited the NF-κB signaling pathway and decreased LPS-induced expression of MUC5AC. Knockdown of p62/SQSTM1 expression reduced activation of the NF-κB signaling pathway and reduced LPS-induced mucus secretion by BEAS-2B cells in vitro. SIGNIFICANCE:In this in vitro study, which utilized BEAS-2B bronchial epithelial cells, p62/SQSTM1 was shown to have a role in LPS-induced mucus hypersecretion by activating the NF-κB signaling pathway.

journal_name

Life Sci

journal_title

Life sciences

authors

Wu Y,Li Y,Wang B,He X,Li Y,Wu B,Yu G,Wang H,Xu B

doi

10.1016/j.lfs.2018.09.030

subject

Has Abstract

pub_date

2018-10-15 00:00:00

pages

270-278

eissn

0024-3205

issn

1879-0631

pii

S0024-3205(18)30583-6

journal_volume

211

pub_type

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