The long-term goal of my laboratory is to understand the molecular mechanisms regulating phenotypic plasticity in smooth muscle cells. Phenotypic plasticity is a phenomenon by which mature contractile smooth muscle cells reversibly switch to an immature synthetic phenotype, which can result in the production of inflammatory mediators coupled with changes in cell numbers and mass. Our laboratory was one of the first to describe miRNA expression in human airway smooth muscle cells and have identified miR-25 as a target of phenotypic plasticity in this cell type. We are currently investigating the mechanisms by which miR-25 and other miRNAs regulate airway smooth muscle phenotype in culture by studying inflammatory, proliferative and contractile functions of airway smooth muscle cells. We are also developing a transgenic animal model of miR-25 expression to study the role of this miRNA on lung function in an animal model of allergic asthma.
We are currently furthering our study of miRNA in other smooth muscle cell types. Our laboratory collaborates with the Myometrial Function Group to explore the regulation of miRNA in human uterine smooth muscle function. The goal of this work is to identify gene-silencing pathways leading to the onset of pre-term labor. We are examining miR-25 function is vascular smooth muscle cells to determine whether miR-25 expression affects smooth muscle phenotypes relevant to cardiovascular disease.
- B.S., 1993, University of Nevada, Reno, Pharmacology
- Ph.D., 1998, University of Washington, Pharmacology