Shannon Conley, Ph.D.
Education
PhD Pharmacology & Toxicology 2005, University of Arizona, Tucson AZ
MPH 2002, University of Arizona, Tucson AZ
BA 2000, University of the South, Sewanee TN
Research Overview
Age-related changes in cerebrovascular fragility
During aging, blood vessels in the brain become fragile leading to loss of vessels as well as small microbleeds. These vascular defects lead to cognitive decline and mobility problems, but the cellular mechanisms underlying them is unknown. Our lab is interested in the role of vascular smooth muscle cells (VSMCs) and pericytes in the development of age-related cerebrovascular fragility. Specifically we are interested in how deficiency in the growth factor IGF-1 may affect VSMCs during aging. Our goal is to understand the cellular mechanisms and transcriptional regulation that cause VSMCs to become defective during aging, leading ultimately to decreased cerebrovascular health.
Mechanisms underlying vascular smooth muscle cell phenotypic plasticity
Vascular smooth muscle cells (VSMCs) are an essential component of vascular homeostasis and vascular function. VSMCs retain a high degree of plasticity and can transition from a contractile to a migratory/synthetic state in response to signaling from a variety of stimuli, including growth factors, mechanical stretch, cholesterol, and oxidative stress. The phenotypic switch to a migratory state is an important part of vascular development, but can lead to pathological changes in various disease states including the vessel remodeling associated with diabetic retinopathy, atherosclerosis, vascularization of tumors, and cerebromicrovascular disease. Much remains unknown about the mechanisms which regulate this phenotypic switch and about the variety of synthetic phenotypes VSMCs can adopt. Our lab is interested in mechanisms underlying regulation of this plasticity, and have identified a variety of factors including transcription factors, guidance proteins, and small GTPases that play a role in this process. We are also interested in understanding what signaling leads to the adoption of some aspects of the synthetic phenotype and not others. These studies are essential to our understanding of VSMC phenotypic switching and provide insight into the regulation of a process that is critical to multiple debilitating diseases.
Conley Lab
Shanon Conley, Ph.D.
Principal Investigator
Lauren Miller
Graduate Student
Morgan Johnston
Research Assistant
Liz Bullen
Research Assistant