Ontology highlight
ABSTRACT: Background
Exposure to ambient fine particulate matter air pollution (PM(2.5); < 2.5 µm in aerodynamic diameter) induces endothelial dysfunction and increases the risk for cardiovascular disease. Endothelial progenitor cells (EPCs) contribute to postnatal endothelial repair and regeneration. In humans and mice, EPC levels are decreased upon exposure to elevated levels of PM(2.5).Objective
We examined the mechanism by which PM(2.5) exposure suppresses circulating levels of EPCs.Methods
Mice were exposed to HEPA-filtered air or concentrated ambient fine particulate matter (CAP, 30-100 µg/m³) from downtown Louisville (Kentucky) air, and progenitor cells from peripheral blood or bone marrow were analyzed by flow cytometry or by culture ex vivo.Results
Exposure o
SUBMITTER: Haberzettl P
PROVIDER: S-EPMC3385427 | biostudies-literature | 2012 Jun
REPOSITORIES: biostudies-literature