Peyton:Research: Difference between revisions
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Cardiovascular disease has been the number one killer in the United States since 1900 for every year except one, and will be responsible for 37% of all deaths in the U.S. this year alone. Arteriosclerosis is defined by hardening of the arteries: a general term for arterial wall thickening and loss of elasticity. Matrix properties in atherosclerotic arteries, such as the existence of macrophages and cytokines from atherosclerotic plaques, arterial wall elasticity, and the portfolio of insoluble adhesive proteins, are altered in the onset of cardiovascular disease. Coincident with these matrix changes, smooth muscle cells (SMCs) are observed to undergo phenotypic dedifferentiation, described by gene transcription, motility/invasion, and matrix degradation/production. We are investigating the ability of matrix state to trigger SMC motility and invasion via a specific signaling network. With a novel set of tools, including biomaterials and a small shRNA library coding for genes important to SMC differentiation and motility, we can control both of the inputs to this hypothesized feedback loop. This research will generate synthetic engineered arterial mimics in which to study the biophysical crosstalk between SMCs and the chemical and physical microenvironment. These studies will lead to identification of druggable signaling nodes, to regulate SMC phenotype in patients with atherosclerosis. | Cardiovascular disease has been the number one killer in the United States since 1900 for every year except one, and will be responsible for 37% of all deaths in the U.S. this year alone. Arteriosclerosis is defined by hardening of the arteries: a general term for arterial wall thickening and loss of elasticity. Matrix properties in atherosclerotic arteries, such as the existence of macrophages and cytokines from atherosclerotic plaques, arterial wall elasticity, and the portfolio of insoluble adhesive proteins, are altered in the onset of cardiovascular disease. Coincident with these matrix changes, smooth muscle cells (SMCs) are observed to undergo phenotypic dedifferentiation, described by gene transcription, motility/invasion, and matrix degradation/production. We are investigating the ability of matrix state to trigger SMC motility and invasion via a specific signaling network. With a novel set of tools, including biomaterials and a small shRNA library coding for genes important to SMC differentiation and motility, we can control both of the inputs to this hypothesized feedback loop. This research will generate synthetic engineered arterial mimics in which to study the biophysical crosstalk between SMCs and the chemical and physical microenvironment. These studies will lead to identification of druggable signaling nodes, to regulate SMC phenotype in patients with atherosclerosis. | ||
[[Image:AHA_Grant. | [[Image:AHA_Grant.jpg|center|300px]] | ||
== Signaling Network-Microenvironment Crosstalk in Metastasis == | == Signaling Network-Microenvironment Crosstalk in Metastasis == |
Revision as of 09:49, 23 January 2011
Matrix Physicochemical Cues as Chemotherapeutic Protective Agents in Hepatocellular CarcinomaThuy Nguyen Inflammatory Feedback Loops in Cardiovascular DiseaseWill Herrick Signaling Network-Microenvironment Crosstalk in MetastasisCollaboration with the Shannon Alford Lab at the University of Minnesota Erinn Dandley
Anomalous Diffusion Methods to Predict 3D Stem Cell Motility in Porous ScaffoldsCollaboration with Joshua Cohen and the Lauffenburger Lab at Massachusetts Institute of Technology Jaclyn Somadelis |