Acute spinal cord injuries are notoriously difficult to
repair, both architecturally and functionally. Unlike injuries in the
peripheral nervous system, those in the spinal cord often result in the
emergence of a severely degenerative local environment, leading to
further tissue damage in the months following the initial insult.
Although much work has been done to identify the causes of this
degenerative environment, there has been relatively little success in
achieving regeneration after a spinal cord injury.
Currently, we are investigating the effect of these scaffold properties on the ability of human microvascular endothelial cells to form angiogenic sprouts within these elastin-based materials. Spinal cord injuries often involve the destruction of vasculature that would provide nutrients and waste transport to the injured area. By identifying the environmental parameters that promote vascular growth and sprouting, we may come one step closer to learning how to engineer a new vasculature that would support the regeneration of the injured spinal cord tissues.