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Effect of Mitochondrial Oxidative Stress and Age on the Signaling Pathway of Ultrafine Particulate Matter Exposure in Murine Aorta
Tong, H., Jackie Carter, AND D. Diaz-Sanchez. Effect of Mitochondrial Oxidative Stress and Age on the Signaling Pathway of Ultrafine Particulate Matter Exposure in Murine Aorta. Presented at 2013 International Conference of the American Thoracic Society, May 17 - 22, 2013.
The data in the abstract decribed the health effects of ultrafine particulate matter.
Epidemiological studies have linked ultrafine particulate matter (PM) exposure and adverse cardiovascular events. PM-induced oxidative stress is believed to be a key mechanism contributing to the adverse short-term vascular effects of air pollution exposure. Advanced age is one factor known to decrease anti-oxidant defense and confer susceptibility to the detrimental vascular effects of PM exposure. We have previously shown that vasomotor effects induced by ultrafine PM exposure are increased in aged mice and enhanced in superoxide dismutase 2 deficient (SOD2+/-) mice having decreased anti-oxidant defense. This study was designed to evaluate the signaling pathway of ultrafine PM exposure in mouse aorta. Thoracic aorta isolated from young (4 m old) and aged (16 m old) wild type (WT) and SOD2+/- mice were exposed to 50 µg/ml Chapel Hill ultrafine PM for 15 min. The activation of MAPK and AKT was assessed by Western blot analysis. We demonstrated that the phosphorylation of p38 and ERK1/2 was increased in the WT aged and SOD2+/- aorta versus WT young control and the WT aged had the greatest increase. In contrast, the phosphorylation of AKT was decreased in the WT aged and SOD2+/- aorta. Furthermore, ultrafine PM treatment enhanced the phosphorylation of p38, ERK1/2, and AKT compared to non-treatment. This study indicates that ultrafine PM-induced MAPK and AKT activation could mediate those vasomotor effects in aged and loss of anti-oxidant defense mice in vitro after ultrafine PM exposure. This abstract of a proposed presentation does not necessarily reflect EPA policy.
Record Details:Record Type: DOCUMENT (PRESENTATION/ABSTRACT)
Organization:U.S. ENVIRONMENTAL PROTECTION AGENCY
OFFICE OF RESEARCH AND DEVELOPMENT
NATIONAL HEALTH AND ENVIRONMENTAL EFFECTS RESEARCH LABORATORY
ENVIRONMENTAL PUBLIC HEALTH DIVISION
CLINICAL RESEARCH BRANCH