Research Interest
Mechanisms of Brain injury and Repair: Cerebrovascular Remodeling, Neurogenesis and NeuroInflammation
- Our laboratory uses a variety of cellular, molecular and imaging tools to investigate Eph receptor biology and function following brain injury. Eph receptors are developmentally important molecules critical for axon growth/guidance molecules, which we discovered play a critical role in regulating injury-induced vascular function, including pial collateral vessel remodeling. This work was recently published in Journal of Clinical Investigations. We routinely evaluate Eph signaling using conditional gene targeted approaches in murine models of stroke and Traumatic brain injury. These tools are being utilized to further uncover the mechanisms underlying neuroinflammation, aberrant neurogenesis and negative behavioral outcomes.
- Toward our long-term translational goal, we have begun testing the effects of several novel Eph receptor blocking peptides for their therapeutic potential in treating brain injury. We are simultaneously developing a nanoparticle system and other delivery methods aimed at limiting the scope of tissue damage, protecting the blood brain barrier and retooling the neuroinflammatory response.
Current Funding
NIH R01 Novel Cellular and Molecular Regulation of Collateral Remodeling in Ischemic Stroke
NIH R01 Novel Cellular and Molecular Regulation of Collateral Remodeling in Ischemic Stroke
NIH R01 Novel Cellular and Molecular Regulation of Collateral Remodeling in Ischemic Stroke
Coronary and cerebrovascular disease remains the leading cause of morbidity and mortality in the US, afflicting more than 1.8 million Americans each year. Ischemic injury following vascular occlusion is often dictated by the extent and remodeling of pre-existing pial collateral or "by-pass" vessels. Our overall goal is to improve collateral remodeling and to understand how this influences the microenvironment in which neurons repair themselves. Novel insights into this important adaptive response will help advance collaterotherapeutics for neurorestoration after stroke.
NIH R01 Mechanisms Regulating Cerebral Arteriogenesis and Neurorestoration
NIH R01 Novel Cellular and Molecular Regulation of Collateral Remodeling in Ischemic Stroke
NIH R01 Novel Cellular and Molecular Regulation of Collateral Remodeling in Ischemic Stroke
Promoting vascular remodeling has emerged as a potential therapeutic approach for neurorestorative therapy. Cerebral vascular trauma leads to inadequate cerebral blood flow which potentiates neuronal cell loss resulting in motor and cognitive deficits in models of brain injury. Endothelial cells lining the blood vessels actively respond to tissue trauma. Our novel findings demonstrate, cell-to-cell contact proteins called Eph receptors are present on cerebral arterioles and play a central role in limiting vascular function following traumatic brain injury.
Virginia Tech leads $2.6 million study of brain trauma, epilepsy connection
NIH R01 Novel Cellular and Molecular Regulation of Collateral Remodeling in Ischemic Stroke
Virginia Tech leads $2.6 million study of brain trauma, epilepsy connection
Virginia Tech is launching a $2.6 million study to determine if traumatic brain injuries can cause changes within the brain that lead to epilepsy. Funded by the nonprofit Citizens United for Research in Epilepsy (CURE) and the U.S. Department of Defense, the three-year study seeks to identify the root causes behind why a person may develop epilepsy after he or she has suffered brain trauma, including sports-related concussion and focal contusion injuries.