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Cell Culture: We use primary cultures of smooth muscle cells, cardiomyocytes and myoblasts to assess cell growth, motility differentiation, and fusion using state-of-the-art approaches to track these processes in real-time.

Mouse Genetics: To dissect the requirement for adhesion signals in cardiac development and disease, our laboratory has generated several animal models with cardiac-, skeletal muscle- or vascular-specific gain-of-function or loss-of-function expression of FAK, FRNK and FAK-binding partners using either tissue-specific transgenic overexpression or genetic deletion by homologous recombination. Our transgenic approach involves expression of a gene of interest under the indirect control of tissue-specific promoters. This system provides the flexibility to use the same transgenic lines to target expression to the vasculature or to heart (or other specialized cell types) at various times during development by crossing with different cell/tissue-specific Cre lines. We use several sophisticated surgical procedures to interrogate pathogenic processes including aortic banding to induce cardiac hypertrophy, coronary ligation to induce myocardial infarction, and carotid injury to induce vessel restenosis.

Frogs: As a prelude to understanding the capacity of various FAK binding partners to modulate cardiovascular development in vivo, the laboratory often first explores the function of identified proteins in Xenopus laevis by anti-sense morpholino injection, a powerful model system that provides rapid, efficacious, and cost-effective depletion of target mRNAs in developing embryos. These studies are performed in collaboration with Frank Conlon’s lab at UNC.