Transduction of compressive stress by bronchial epithelium

D. J. Tschumperlin, J. M. Drazen

Research output: Contribution to journalConference articlepeer-review

Abstract

The epithelial lining of the asthmatic airway is exposed to compressive stress as a consequence of smooth muscle constriction. We have shown previously that in vitro compression of bronchial epithelial cells stimulates extracellular signal-regulated kinase (ERK) phosphorylation and downstream gene expression. Here we show that inhibition of signaling through the epidermal growth factor receptor (EGFR) with a tyrosine kinase inhibitor (AG1478) or a neutralizing antibody to the ligand-binding domain of the EGFR blocks compression-induced ERK phosphorylation. A metalloprotease inhibitor (Galardin) and a neutralizing antibody to heparin binding epidermal growth factor (HB-EGF), but not EGF, also attenuates the compression-induced ERK activation. Our results demonstrate that compressive activation of the ERK signaling pathway requires signaling through the EGFR, and involves metalloprotease-dependent shedding of HB-EGF.

Original languageEnglish (US)
Pages (from-to)641-642
Number of pages2
JournalAnnual International Conference of the IEEE Engineering in Medicine and Biology - Proceedings
Volume1
StatePublished - Dec 1 2002
EventProceedings of the 2002 IEEE Engineering in Medicine and Biology 24th Annual Conference and the 2002 Fall Meeting of the Biomedical Engineering Society (BMES / EMBS) - Houston, TX, United States
Duration: Oct 23 2002Oct 26 2002

Keywords

  • EGF receptor
  • MAP kinase
  • Mechanotransduction

ASJC Scopus subject areas

  • Signal Processing
  • Biomedical Engineering
  • Computer Vision and Pattern Recognition
  • Health Informatics

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