Ryan Stowers, Ph.D.
Bioengineering and Mechanical Engineering
University of California, Santa Barbara
In the body, cells are surrounded by a scaffolding of biopolymers that provide physical support and biochemical cues, known as the extracellular matrix (ECM). Hydrogel cell culture models have been used to reveal that properties of the ECM, notably matrix stiffness, can regulate a host of cellular behaviors, such as migration, division, differentiation, and even cancer progression. ECM is often viscoelastic, displaying stress relaxation in response to strain, and recapitulating complex aspects of native ECM, such as dynamic remodeling and viscoelasticity, remains challenging. Further, key aspects of mechanotransduction, such as the effect of mechanics on the epigenome, are not well understood. In this talk, I will discuss how matrix stiffness can induce epigenomic remodeling leading to a tumorigenic phenotype in a breast cancer model. I will also describe our work to develop 3D hydrogel platforms that allow for dynamic tuning of matrix viscoelasticity to better understand the biological impact and pathways involved in mechanotransduction.
Dr. Ryan Stowers is an assistant professor in the Departments of Bioengineering and Mechanical Engineering at the University of California, Santa Barbara. He obtained his B.S. in Bioengineering from Clemson University and his Ph.D. in Biomedical Engineering from the University of Texas at Austin in the laboratory of Dr. Laura Suggs. Following his doctoral research, Dr. Stowers was an NIH Ruth L. Kirschstein postdoctoral fellow in the Department of Mechanical Engineering at Stanford University in the laboratory of Dr. Ovijit Chaudhuri. Dr. Stowers is the recipient of Young Investigator Awards from the Breast Cancer Alliance and Hellman Family Faculty Fellow. His research focuses on developing 3D hydrogel cell culture platforms to mimic native extracellular matrix properties and utilizing these platforms to determine molecular mechanisms by which extracellular matrix regulates cell phenotype.