Enolase is a multifunctional
protein, which is expressed abundantly in the cytosol. Upon stimulatory signals,
enolase can traffic to cell surface and contribute to different pathologies including injury, autoimmunity,
infection,
inflammation, and
cancer. Cell-surface expression of
enolase is often detected on activated macrophages, microglia/macrophages, microglia, and astrocytes, promoting extracellular matrix degradation, production of pro-inflammatory
cytokines/
chemokines, and invasion of inflammatory cells in the sites of injury and
inflammation. Inflammatory stimulation also induces translocation of
enolase from the cytosolic pool to the cell surface where it can act as a
plasminogen receptor and promote extracellular matrix degradation and tissue damage.
Spinal cord injury (SCI) is a devastating debilitating condition characterized by progressive pathological changes including complex and evolving molecular cascades, and insights into the role of
enolase in multiple inflammatory events have not yet been fully elucidated. Neuronal damage following SCI is associated with an elevation of
neuron specific enolase (NSE), which is also known to play a role in the pathogenesis of hypoxic-ischemic
brain injury. Thus, NSE is now considered as a
biomarker in ischemic brain damage, and it has recently been suggested to be a
biomarker in
traumatic brain injury (TBI),
stroke and
anoxic encephalopathy after
cardiac arrest and acute SCI as well. This review article gives an overview of the current basic research and clinical studies on the role of multifunctional
enolase in neurotrauma, with a special emphasis on NSE in acute SCI.