The Reinhart-King Lab investigates tissue formation and the disruption of tissue architecture during disease progression. The environment surrounding cells is a complex milieu of chemical and mechanical signals that direct cell function. We study how cells integrate multiple extracellular signals and translate them into either normal or diseased behaviors.

We use a multidisciplinary approach, integrating principles from engineering, cell and molecular biology, biophysics, microfabrication and biomaterial science, to better understand and control cell function, tissue formation, and disease progression.  We are applying this approach and these tools to understand the progression of cancer and cardiovascular disease, the two leading causes of death in the US.


Cancer and Tissue Engineered Models of Metastasis

MetastasisDuring 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.


AngiogenesisAngiogenesis 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.



AnthereosclerosisAtherosclerosis 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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