Reinhart-King Laboratory

Multidisciplinary approaches to understanding cellular mechanics and cell-biomaterial interactions

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The Reinhart-King lab uses tissue engineering, microfabrication, novel biomaterials, model organisms, and tools from cell and molecular biology to study the effects of mechanical and chemical changes in tissues during disease progression. We have projects focused on cancer, diabetes, cardiovascular disease, and ocular diseases.

We work with scientists and engineers across campus, and we collaborate with clinicians in the world-class Vanderbilt University Medical Center.

Cancer and Tissue Engineered Models of Metastasis
During tumor progression, mechanical, chemical and structural changes occur within the extracellular matrix. It is thought that these changes in the microenvironment may promote malignancy and metastasis. To understand how the physical properties of the tumor microenvironment facilitate the escape of metastatic cells from the primary tumor, we create models of the tumor microenvironment using native and synthetic matrices, microfabricated devices, and novel biomaterials. This work will uncover new therapeutic targets designed to prevent metastasis.
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Angiogenesis is the formation of new capillaries from pre-existing ones and is critical to tumor growth. While much is known about the growth factors and associated signaling pathways that trigger and regulate angiogenesis, less is known about the role of mechanical cues in angiogenesis. Our lab has recently demonstrated that changes in the mechanical properties of the extracellular environment can disrupt the formation of newly forming vascular networks. In this project, we use a combination of in vitro and in vivo models to explore how we can control angiogenesis by manipulating the extracellular environment.
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Atherosclerosis is characterized by the formation plaques within the blood vessel wall that can result in myocardial infarction and/or stroke. Atherosclerosis is intimately linked with age, however it is not clear how aging leads to atherosclerosis. Using both in vitro and ex vivo models of aging, we have recently identified a mechanism by which the natural process of aging leads to atherosclerosis through changes in the extracellular matrix. In this project, we are seeking to inhibit the progression of atherosclerosis with age by targeting the cellular response to mechanical and chemical changes within the blood vessel wall.
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