Robert Mecham, PhD

Alumni Endowed Professor of Cell Biology & Physiology

Cell-matrix interactions, extracellular matrix and development, vascular development and disease Read More

Lab Phone: (314) 362-2254
Website: Mecham Lab
Lab Location: 4616 Cancer Research Bldg
Keywords: extracellular matrix, vascular biology, development, physiology, proteomics

Cell-matrix interactions, extracellular matrix and development, vascular development and disease

A major goal of our research is to understand the complex process of extracellular matrix (ECM) secretion and assembly, with a particular focus on ECM proteins important to the cardiovascular system. We are interested in how ECM macromolecules assemble into complex polymers in the extracellular space, and how ECM influences the phenotype of cells, including the role of ECM in initiating differentiation and in maintaining appropriate gene expression in the differentiated phenotype. Our research involves identifying biologically active signals within ECM molecules that act directly on cell function. These studies include an interest in receptors for extracellular matrix.

The laboratory also has had a long-standing interest in vascular development and disease, particularly in understanding the development of the vessel wall and the recruitment and differentiation of smooth muscle cells. Gene array technology is used to identify genes differentially expressed in developing vessels and in response to hypertension. Using knockout and transgenic mice, we study how the overexpression or underexpression of key vascular wall proteins influences the development and function of the cardiovascular system. Gene arrays, in situ hybridization, and proteomic approaches are used to characterize vascular alteration associated with each animal phenotype, and physiological studies (vascular compliance, vascular reactivity, blood pressure, etc.) are used to document altered vascular function. We are also interested in human inherited diseases involving proteins of the elastic fiber, including supravalvar aortic stenosis (linked to mutations in the elastin gene), Marfan Syndrome (associated with mutations in fibrillin), and pulmonary and systemic hypertension.

Updated April 2014