Science Inventory

ASBESTOS-INDUCED ACTIVATION OF CELL SIGNALING PATHWAYS IN HUMAN BRONCHIAL EPITHELIAL CELLS

Citation:

WANG, X., J. M. SAMET, AND A. J. GHIO. ASBESTOS-INDUCED ACTIVATION OF CELL SIGNALING PATHWAYS IN HUMAN BRONCHIAL EPITHELIAL CELLS. EXPERIMENTAL LUNG RESEARCH. Taylor & Francis, Inc., Philadelphia, PA, 19(8):1044-1050, (2006).

Impact/Purpose:

To determine whether the activation of the epidermal growth factor (EGF) receptor signal pathway after asbestos exposure involves an oxidative stress

Description:

Using respiratory epithelial cells transfected with either superoxide dismutase (SOD) or catalase, the authors tested the hypothesis that the activation of the epidermal growth factor (EGF) receptor signal pathway after asbestos exposure involves an oxidative stress. Western blotting using phospho-specific antibodies demonstrated that the EGF receptor kinase inhibitor PD153035 decreased both the phosphorylation of extracellular signal-regulated kinase (ERK)1/2 and its upstream signal pathway, including mitogen-activate protein kinase/ERK kinase (MEK)1/2. Similarly, the MEK1/2 kinase inhibitor PD98059 also demonstrated the ability to decrease phosphorylation of ERK1/2. Crocidolite-induced phosphorylation of EGF receptor, ERK1/2, and MEK1/2 was reduced by transfection of BEAS-2B cells with a catalase vector, supporting a participation of oxidative stress in this pathway. These results show that crocidolite can activate the phosphorylation of EGF receptor and its downstream cell signal pathway in BEAS-2B cells and this is associated with the oxidative stress presented by the fibers.

Record Details:

Record Type: DOCUMENT (JOURNAL/PEER REVIEWED JOURNAL)
Product Published Date: 10/08/2006
Record Last Revised: 07/14/2008
OMB Category: Other
Record ID: 166791

Organization:

U.S. ENVIRONMENTAL PROTECTION AGENCY

OFFICE OF RESEARCH AND DEVELOPMENT

NATIONAL HEALTH AND ENVIRONMENTAL EFFECTS RESEARCH LABORATORY

HUMAN STUDIES DIVISION

IMMEDIATE OFFICE