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Mitogen-activated protein kinase involves neutrophil elastase-induced morphological changes in human bronchial
S Hashimoto1, S Maruoka, Y Gon
1First Department of Internal Medicine, Nihon University School of Medicine, Tokyo, Japan. shuh@nihon-u.ac.jp
Life Sciences
|May 13, 1999
Summary
Neutrophil elastase (NE) causes airway epithelial cells to detach by activating the MAPK pathway, which alters cell morphology. Inhibiting this pathway with PD 98059 reduced these NE-induced effects.
Area of Science:
- Cell Biology
- Respiratory Medicine
- Biochemistry
Background:
- Neutrophil elastase (NE) is known to cause airway epithelial cell detachment.
- The Ras/Raf-initiated mitogen-activated protein kinase (MAPK) pathway regulates cell adhesion and morphology.
- The specific role of MAPK in NE-induced changes in bronchial epithelial cell (BEC) morphology is not well understood.
Purpose of the Study:
- To investigate the involvement of the MAPK pathway in NE-induced morphological changes and detachment of BEC monolayers.
- To determine if inhibiting the MAPK pathway affects NE-induced cellular alterations.
Main Methods:
- BEC monolayers were stimulated with NE.
- Changes in cellular morphology and MAPK activation were assessed.
- The effect of PD 98059, a specific inhibitor of MAPK kinase-1 (MEK-1), on NE-induced effects was evaluated.
Main Results:
- NE stimulation led to BEC detachment and gap formation, accompanied by MAPK activation.
- PD 98059 treatment attenuated both the morphological changes and MAPK activation induced by NE.
- These findings suggest a role for the MAPK pathway beyond NE's proteolytic activity on the extracellular matrix.
Conclusions:
- The MAPK pathway is partially involved in NE-induced changes in BEC monolayer morphology and cell detachment.
- NE-activated MAPK signaling contributes to the disruption of bronchial epithelial cell integrity.