Cadmium induces mucin 8 expression via Toll-like receptor 4-mediated extracellular signal related kinase 1/2 and p38 mitogen-activated protein kinase in human airway epithelial cells

International Forum of Allergy & Rhinology
Si-Youn SongYong-Dae Kim

Abstract

Inhalation of cadmium can lead to development of inflammatory airway diseases such as acute pulmonary edema and chronic obstructive pulmonary disease. In inflammatory airway diseases, expression of mucins is increased, which leads to increased morbidity and mortality of the affected patients. However, no study on the effect of cadmium on expression of mucin genes in airway epithelial cells has been reported. Therefore, this study was conducted in order to investigate the effect and the brief signaling pathway of cadmium on expression of mucin genes in human airway epithelial cells. In mucin-producing human NCI-H292 airway epithelial cells and primary cultures of normal nasal epithelial cells, the effect and signaling pathway of cadmium on expression of mucin genes were investigated using reverse transcription-polymerase chain reaction (RT-PCR), real-time PCR, enzyme immunoassay, and immunoblot analysis with several specific inhibitors and small interfering RNA (siRNA). Cadmium increased mucin 8 (MUC8) expression and Toll-like receptor (TLR) 4 messenger RNA (mRNA) expression. Cadmium significantly activated phosphorylation of extracellular signal related kinase 1/2 (ERK1/2) mitogen-activated protein kinase (MAPK) and p38 MAPK. E...Continue Reading

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Citations

Jun 28, 2016·International Forum of Allergy & Rhinology·David W Kennedy
Feb 9, 2018·Journal of Clinical Medicine·Hee-Jae Cha, Kyoung Seob Song
Dec 4, 2019·Immunopharmacology and Immunotoxicology·Nikoo Hossein-KhannazerMohammad Noorisepehr
May 28, 2019·Frontiers in Immunology·Doumet Georges HelouSaadia Kerdine-Römer

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