Gene expression changes after focal stroke, traumatic brain and spinal cord injuries

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Purpose of review

Large-scale gene expression profiling has recently been performed on stroke and spinal cord injuries. These studies provide insights into coordinated patterns of gene expression within the injury and the interrelationships of neurodegenerative and neural repair processes after injury.

Recent findings

The molecular signals for post-stroke angiogenesis begin within hours of initial cerebral ischemia, with sequential increases in message for initially destabilizing combinations of vascular growth factors and growth factor receptors, followed by growth factor combinations that promote endothelial cell division and stabilization. The overlap in molecular signaling between post-stroke angiogenesis, neurogenesis and axonal sprouting suggests a continuum of vascular and neural reorganization in the tissue adjacent to stroke. Inflammation after injury extends through early and late changes in the cytokine message. SOCS-3, a negative regulator of cytokine signaling, is increased after injury and may be neuroprotective. Components of an adult neuronal growth program have been identified in the peripheral nervous system during axonal regeneration, with overlap to axonal sprouting after stroke. The gene expression profile of the aged brain suggests an altered central nervous system environment that may exacerbate initial injury and impair neural reorganization after stroke and spinal cord injury.


When rigorously tested and independently validated, data from large-scale gene expression analyses provide new insights into the aggregate genetic control of stroke and spinal cord injury, and the interrelationship of important cellular events within the damaged region. These data also highlight novel genes in these processes, and suggest new directions in the investigation of tissue reorganization and repair after central nervous system injury.

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