Research Interest
Mechanisms of Brain injury and Repair: Cerebrovascular Remodeling, Neurogenesis and NeuroInflammation
- Our laboratory studies Eph receptor biology and function following brain injury. Eph receptors are developmentally important molecules critical for axon growth & guidance , which we discovered play a critical role in regulating injury-induced vascular remodeling. This work was recently published in the Journal of Clinical Investigation. We interrogate Eph signaling using conditional gene targeted approaches in murine models of stroke, traumatic brain injury and post-traumatic epilepsy. We use a variety of cellular, molecular and advanced imaging tools to further our investigations with an emphasis on neurovascular and neuroimmune health.
- Toward our long-term translational goal, we have begun testing 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 extend of tissue damage, protecting the blood brain barrier and retooling the neuroinflammatory milieu.
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
Ischemic injury following vascular occlusion is often dictated by 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.
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. New insights into the regulation of cerebral vascular trauma will aid our understanding of the impact of TBI on cerebral blood flow loss, which potentiates neuronal cell loss resulting in motor and cognitive deficits in models of 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.
NIH R01 Age-dependent peripheral innate immunity in TBI
NIH R01 Mechanisms suppressing pro-resolving innate immunity inTBI
Virginia Tech leads $2.6 million study of brain trauma, epilepsy connection
There is a paucity of data that limits our understanding of innate immune regulation across the age spectrum following TBI. Exploiting the pro-resolving phenotype of young innate immune cells may provide a novel restorative intervention aimed at improving TBI outcomes and reveal novel targets for drug discovery.
NIH R01 Mechanisms suppressing pro-resolving innate immunity inTBI
NIH R01 Mechanisms suppressing pro-resolving innate immunity inTBI
NIH R01 Mechanisms suppressing pro-resolving innate immunity inTBI
Limited information exists pertaining to the physiological relevance of innate immune regulation and the key players driving their phenotypic response following TBI. Completion of these studies will advance our understanding of how peripheral-derived monocyte/macrophages dictates neurovascular injury and recovery in the pathophysiology of TBI.