University of Louisville
Environmental Pollutants and Obesity: Effects on Circulating and Bone Marrow Endothelial Progenitor Cells
Institution
University of Louisville
Faculty Advisor/ Mentor
Daniel Conkin; Petra Haberzettl
Abstract
Environmental air pollutants, such as fine particulate matter (PM2.5), are associated with increased risk of cardiovascular disease (CVD) and mortality. Obesity is an emerging epidemic in the United States and is associated with increased risk for the development of diabetes and CVD. Endothelial progenitor cells (EPCs) contribute to endothelium health and are important in angiogenesis and endothelial repair, and the levels of EPCs in the blood are a prognostic indicator for cardiovascular health. This study was designed to investigate the effects of diet induced obesity (DIO) and exposure to PM2.5 on murine endothelial progenitor cell populations. C57BL/6 mice were exposed to concentrated air particulate matter (CAP, 6-10x concentrated ambient PM2.5, 6h/d, 4, 9, or 30 days), and/or fed high fat diet (60% kcal from fat, 4 or 12 weeks). Mice exposed to PM2.5 showed a significant decrease in peripheral blood EPC (PB EPC) levels, measured as Flk-1+/Sca-1+ cells by flow cytometry. The decrease in circulating EPCs was accompanied by an increase in bone marrow derived cells (BMDCs), positive for Flk1+/Sca-1+ and DiI-acLDL+/UE-lectin+ as measured by immunoflourescence microscopy. DIO also decreases PB EPC levels, and increases the number of bone marrow derived Flk-1+/Sca-1+ and DiI-acLDL+/UE-lectin+ cells. When high fat fed mice were exposed to PM2.5, we found a decrease in PB EPCs, along with an increase in BMDCs. However, combination of PM2.5 and HFD had no significant additive effect on EPC numbers. These results indicate that PM2.5 and DIO impair EPC mobilization from the bone marrow in a similar, non-additive way.
Environmental Pollutants and Obesity: Effects on Circulating and Bone Marrow Endothelial Progenitor Cells
Environmental air pollutants, such as fine particulate matter (PM2.5), are associated with increased risk of cardiovascular disease (CVD) and mortality. Obesity is an emerging epidemic in the United States and is associated with increased risk for the development of diabetes and CVD. Endothelial progenitor cells (EPCs) contribute to endothelium health and are important in angiogenesis and endothelial repair, and the levels of EPCs in the blood are a prognostic indicator for cardiovascular health. This study was designed to investigate the effects of diet induced obesity (DIO) and exposure to PM2.5 on murine endothelial progenitor cell populations. C57BL/6 mice were exposed to concentrated air particulate matter (CAP, 6-10x concentrated ambient PM2.5, 6h/d, 4, 9, or 30 days), and/or fed high fat diet (60% kcal from fat, 4 or 12 weeks). Mice exposed to PM2.5 showed a significant decrease in peripheral blood EPC (PB EPC) levels, measured as Flk-1+/Sca-1+ cells by flow cytometry. The decrease in circulating EPCs was accompanied by an increase in bone marrow derived cells (BMDCs), positive for Flk1+/Sca-1+ and DiI-acLDL+/UE-lectin+ as measured by immunoflourescence microscopy. DIO also decreases PB EPC levels, and increases the number of bone marrow derived Flk-1+/Sca-1+ and DiI-acLDL+/UE-lectin+ cells. When high fat fed mice were exposed to PM2.5, we found a decrease in PB EPCs, along with an increase in BMDCs. However, combination of PM2.5 and HFD had no significant additive effect on EPC numbers. These results indicate that PM2.5 and DIO impair EPC mobilization from the bone marrow in a similar, non-additive way.