Molecular Regulators of Myofibroblast Differentiation and Fibrosis
Jennifer Davis (Joint Pathology/BioE Faculty Candidate)
Cincinnati Children's Hospital/Howard Hughes Medical Institute
January 12, 2015
Foege N130A, Wallace H. Coulter Seminar Room
Fibrosis, which is a specialized extracellular matrix-based scar tissue, occurs with virtually every form of heart disease that is both a hemodynamic burden but also a strong prognostic indicator of heart failure. In addition the limited regenerative capacity of the myocardium dictates that the injury response solely results in a permanent fibrotic scar, which further exacerbates the loss of cardiac function and creates a myocardial environment that is hostile to regeneration. The material that causes scarring is primarily released from specialized cells called myofibroblasts, which become activated in response to injury. Through the use of in-cell genome-wide screening and genetic engineering at both the cellular and organismal levels we’ve been uncovering the molecular signaling networks that result in myofibroblast differentiation along with the contribution of these specialized cells to the cardiac injury response. The identification of these regulatory networks should in turn present molecular targets that can be leveraged for pharmacologic intervention to enhance repair or block the fibrotic response.
Dr. Jennifer Davis received her Ph.D. in Molecular & Integrative Physiology at the University of Michigan, followed by postdoctoral training at the Cincinnati Children’s Hospital Heart Institute in the laboratory of Dr. Jeffery Molkentin. She is currently a Research Faculty member there, has received a K99/R00 transitional award from the NIH and was recently the recipient of the Louis N. & Arnold M. Katz Award from the American Heart Association. Her work focuses on the cellular & molecular mechanisms of cardiac repair and fibrosis using gene and cellular engineering approaches, with the goal of developing novel therapies for heart failure.