Nat Med, 2012 · DOI: 10.1038/nm.2990 · Published: November 1, 2012
Acute central nervous system (CNS) injury induces damage but also a process of delayed tissue repair. Neural repair involves remodeling the boundaries of the lesion, forming new blood vessels, elaborating new neuronal connections and generating new populations of neurons and glia. The formation of new blood vessels through sprouting from preexisting vessels1, a phenomenon called angiogenesis, occurs in stroke, traumatic brain and spinal cord injury, and multiple sclerosis during the repair phase of the disease process2,3. In this issue of Nature Medicine, Muramatsu et al.5 use a highly targeted inflammatory injury to the thoracic spinal cord that damages descending corticospinal tract (CST) projections from the brain to model some aspects of human multiple sclerosis.
The finding that neovessel-derived prostacyclin induces local axonal sprouting and functional recovery in other CNS injury and regeneration models, then this might be clinically targeted with focal delivery of prostacyclin agonists into recovering tissue.
Tissue repair after acute CNS injury occurs in a unique cellular environment adjacent to the injury site that involves cellular events not normally active in most brain areas— angiogenesis is linked to neurogenesis in an area of active axonal sprouting and tissue remodeling.
Angiogenic blood vessels are a rich tissue source for secreted and membrane-bound signaling molecules that have been shown to form instructive vascular niches in cancer and peripheral injury environments.