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The overall goal of the Small lab is to better understand the mechanisms that control cell identity and lineage commitment by studying the transcriptional regulation and function of cardiac tissue-restricted genes. Our motivation is to decipher how disruption of cardiac gene expression programs in heart disease contributes to cellular pathophysiology and the decline in cardiac function. There are two major themes of research within the lab that we study using mouse genetics, cell biology, advanced imaging, bioinformatic and biochemical approaches:
A. Histological sections from the left ventricle of mice subjected to sham surgery or myocardial infarction were immunostained with antibodies to visualize GFP-positive fibroblasts (green), cTNT-positive cardiomyocytes (purple) and DAPI-positive nuclei (blue). Note expansion of fibroblasts in ischemic myocardium.
B. Cultured epicardial cells were immunostained with antibodies to visualize ZO1 positive cell adhesions (green), ACTA2-positive stress fibers (red) and DAPI-positive nuclei (blue). Note the tightly packed cobble-stoned morphology of epicardial cells in quiescent cultures and the loss of adhesions and accumulation of robust stress fibers in epicardial cells being mobilized to undergo epicardium-to-mesenchymal transition.
Eric M. Small, Ph.D.
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