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The D’Amore laboratory has a long history of interest in understanding vascular development and pathology, particularly as it relates to the retina in pathologies such as diabetic retinopathy and wet age-related macular degeneration.  Over the past two decades she has focused on the role of VEGF in these process and she and her colleagues contributed to the work that forms the basis for the use of anti-VEGF therapies in the eye.

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Our laboratory is interested in understanding the cellular and molecular constituents of hematopoietic stem cell niche. We have identified differential functions of vascular niches in the bone marrow.

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Research in the Milewicz laboratory has three components. The first component is recruiting and clinically characterizing families with multiple members with vascular disease, including thoracic aortic aneurysms, acute aortic dissections, cerebral aneurysms, and early onset ischemic strokes.

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A major focus of our research program is the role of the extracellular matrix (ECM) in cardiovascular homeostasis and disease. We are pursuing our studies using mouse models of Marfan syndrome (MFS), a multi-system disease caused by mutations in the ECM component and TGFβ regulator fibrillin-1, and a combination of genetic, pharmacological, ex vivo and computational approaches.

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My research program studies physiological functions and pathological alterations in ion channels in arterial smooth muscle cells. A major focus is to understand mechanisms by which ion channels control arterial contractility.

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Our lab is interested in the transcriptional regulation of genes that impact vascular development and maintenance. We specifically study ATP-dependent chromatin-remodeling complexes, which transiently modulate chromatin to facilitate transcriptional regulation.

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The primary objective of the lab is to understand how clinical risk factors such as insulin resistance and hyperinsulinemia trigger endothelial dysfunction and associated vasculopathies. Our focus for the last seven years has been to understand the involvement of protein tyrosine phosphatases in endothelial inflammation and dysfunction.

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The goal of my research is to bridge bench to bedside to gain understanding of mechanisms responsible for athero-thrombotic and other vascular diseases, including angiogenesis. Our focus for nearly 25 years has been the vascular biology of the type B scavenger receptor CD36.

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