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Hog barn dust slows airway epithelial cell migration in vitro through a PKCalpha-dependent mechanism.

Authors
Slager-RE; Allen-Gipson-DS; Sammut-A; Heires-A; DeVasure-J; Von Essen-S; Romberger-DJ; Wyatt-TA
Source
Am J Physiol, Lung Cell Mol Physiol 2007 Dec; 293(6):L1469-L1474
NIOSHTIC No.
20033205
Abstract
Agricultural work and other occupational exposures are responsible for approximately 15% of chronic obstructive pulmonary disease (COPD). COPD involves airway remodeling in response to chronic lung inflammatory events and altered airway repair mechanisms. However, the effect of agricultural dust exposure on signaling pathways that regulate airway injury and repair has not been well characterized. A key step in this process is migration of airway cells to restore epithelial integrity. We have previously shown that agents that activate the critical regulatory enzyme protein kinase C (PKC) slow cell migration during wound repair. Based on this observation and direct kinase measurements that demonstrate that dust extract from hog confinement barns (HDE) specifically activates the PKC isoforms PKCalpha and PKCepsilon, we hypothesized that HDE would slow wound closure time in airway epithelial cells. We utilized the human bronchial epithelial cell line BEAS-2B and transfected BEAS-2B cell lines that express dominant negative (DN) forms of PKC isoforms to demonstrate that HDE slows wound closure in BEAS-2B and PKCepsilon DN cell lines. However, in PKCalpha DN cells, wound closure following HDE treatment is not significantly different than media-treated cells. These results suggest that the PKCalpha isoform is an important regulator of cell migration in response to agricultural dust exposure.
Keywords
Worker-health; Work-environment; Occupational-hazards; Safety-measures; Lung-burden; Lung-irritants; Bronchial-asthma; Dust-particles; Dusts; Agricultural-workers; Lung-cells; Cell-biology; Cell-function; Cell-migration; Respiratory-system-disorders; Pulmonary-system-disorders
Contact
Rebecca E. Slager, Department of Internal Medicine, Pulmonary and Critical Care Medicine Section, University of Nebraska Medical Center, Omaha, NE 68198-5300
CODEN
APLPE7
Publication Date
20071201
Document Type
Journal Article
Funding Type
Grant
Fiscal Year
2008
NTIS Accession No.
NTIS Price
Identifying No.
Grant-Number-R01-OH-008539
Issue of Publication
6
ISSN
1040-0605
Priority Area
Agriculture, Forestry and Fishing
Source Name
American Journal of Physiology: Lung Cellular and Molecular Physiology
State
NE
Performing Organization
University of Nebraska
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