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Neutrophil elastase causes MUC5AC mucin synthesis via EGF receptor, ERK and NF-kB pathways in A549 cells

Jeong-Sup Song1, Kyung-Sook Cho, Hyung-Kyu Yoon

  • 1Department of Internal Medicine, St Mary's Hospital, The Catholic University of Korea College of Medicine, Seoul, Korea. jssong@catholic.ac.kr

The Korean Journal of Internal Medicine
|February 24, 2006
PubMed
Abstract

Insights

Neutrophil elastase (NE) upregulates MUC5AC mucin expression via the epidermal growth factor receptor (EGF-R), ERK, and NF-kB pathways in bronchial cells.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Respiratory Medicine

Background:

  • Neutrophil elastase (NE) is known to increase respiratory mucin gene MUC5AC expression.
  • The precise molecular mechanisms underlying this NE-induced MUC5AC upregulation remain unclear.

Purpose of the Study:

  • To elucidate the signal transduction pathway through which NE induces MUC5AC gene expression in bronchial epithelial cells.

Main Methods:

  • Utilized luciferase reporter assays to measure MUC5AC promoter activity in A549 cells following NE stimulation.
  • Employed Western blotting to confirm mitogen-activated protein kinase (MAPK) involvement.
  • Used site-directed mutagenesis and electrophoretic mobility shift assay (EMSA) to investigate nuclear factor-kappaB (NF-kB) activation.
  • Confirmed MUC5AC mRNA expression changes via RT-PCR.

Main Results:

  • NE significantly increased MUC5AC promoter transcriptional activity in A549 cells.
  • This increase was correlated with elevated NF-kB activity, as evidenced by site-directed mutagenesis and EMSA.
  • Extracellular signal-regulated kinases (ERK) were identified as the specific MAPK involved in NE-induced MUC5AC expression.
  • NE stimulation led to increased MUC5AC mRNA levels.

Conclusions:

  • Human NE induces MUC5AC mucin expression in A549 cells.
  • This induction is mediated by a signaling cascade involving the epidermal growth factor receptor (EGF-R), ERK, and NF-kB pathways.

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