Vascular Programming Lab
Our lab is focused on understanding how maternal nutritional status during pregnancy affects the health of the offspring’s cardiovascular system. Specifically, we are focused on studying the function of arteries that are important in blood pressure regulation and how the components of these blood vessels – smooth muscle cells, endothelial cells and perivascular adipose tissue – function together in health and disease.
Ongoing Project descriptions
Maternal Obesity and Offspring Vascular Function
Currently, many women entering pregnancy are either overweight or obese and it is well-established that exposure to maternal obesity during gestation is associated with increased risk of offspring obesity and cardiovascular disease. A major area of investigation in our lab is to understand how maternal factors during pregnancy affect the function and development of the offspring cardiovascular system. Perivascular adipose tissue (PVAT) is a fat depot surrounding blood vessels and is an important paracrine regulator of smooth muscle and endothelial cell function. While studies suggest that PVAT is a key link between obesity and cardiovascular disease, there is a lack of information regarding how maternal nutritional status, dietary factors and physical activity affect offspring PVAT function and overall vascular reactivity. We utilize a wide range of experimental approaches including animal models, isolated vessel contractility, cell culture, molecular biology and genomics. Specifically, we are examining PVAT and arterial function in the offspring of obese mothers with an overall objective of providing a mechanistic understanding of how the in utero environment programs offspring vascular function.
Early growth response 1 (Egr1) and Arterial Function
The immediate early transcription factor early growth response 1 (Egr1) is upregulated in smooth muscle cells of atherosclerotic plaques and in adipose tissue of obese animals and humans. Ca2+ influx via voltage-gated Ca2+ channels is a critical component of smooth muscle contraction, and other groups have shown that Ca2+ influx via voltage-gated Ca2+ channels upregulates Egr1 expression. Using blood vessels from Egr1 knockout mice, our preliminary arterial contractility data suggest that smooth muscle Egr1 may play a role in modulating vascular tone. Current studies are focused on elucidating the signaling pathways and molecular mechanisms that link Egr1 to smooth muscle contractility. It remains to be determined if these pathways are developmentally-regulated, and if they are impacted by diet or physical activity.