Spinal Cord Regeneration

Spinal cord injuries (SCIs) often result in permanent disability with tremendous life-changing impact on individuals and their families. Recent estimations by the National Spinal Cord Injury Statistical Center suggest that more than 302,000 people are living with SCI in the U.S., with approximately 18,000 new cases per year according to 2023 National Spinal Cord Injury Statistical Center (NSCISC) statistics. Significant progress has been made in the care, rehabilitation and survival of individuals with SCI. However, the complexity of SCI's pathophysiology underscores the necessity for continued research to better understand how the injury changes over time and to identify new targets for therapies that will enhance neural plasticity and promote regeneration to foster even greater improvements in functional recovery.

The Neuroregeneration and Neurorehabilitation Lab discovered that genetic blockade of the thrombin receptor protease-activated receptor 1, (PAR1), or protease-activated receptor 2 (PAR2) improves recovery of function across multiple models of spinal cord injury. Ongoing research is focused on the mechanisms that underpin these benefits and their relevance to chronic injury. In addition, the lab's team is focused on the rationale design and implementation of pharmacological strategies that can be provided alone or in conjunction with other interventions to restore function.

Related publications

• PARting neuroinflammation with protease-activated receptor 2 pepducins.
• The thrombin receptor links brain derived neurotrophic factor to neuron cholesterol production, resiliency and repair after spinal cord injury.
• The thrombin receptor modulates astroglia-neuron trophic coupling and neural repair after spinal cord injury.
• Microenvironment proteinases, proteinase-activated receptor regulation, cancer and inflammation.
• Kallikrein-related peptidase 6 orchestrates astrocyte form and function through proteinase activated receptor-dependent mechanisms.
• Targeting the thrombin receptor modulates inflammation and astrogliosis to improve recovery after spinal cord injury.
• Genetic targeting of protease-activated receptor 2 reduces inflammatory astrogliosis and improves recovery of function after spinal cord injury.
• Kallikrein cascades in traumatic spinal cord injury: In vitro evidence for roles in axonopathy and neuron degeneration.
• Kallikrein 6 signals through PAR1 and PAR2 to promote neuron injury and exacerbate glutamate neurotoxicity.
• Kallikrein 6 is a novel molecular trigger of astrogliosis.     
• Functional role of kallikrein 6 in regulating immune cell survival. 
• Activation profiles of human kallikrein-related peptidases by matrix metalloproteinases.