Metabolic Brain Disease

, Volume 31, Issue 3, pp 487–495 | Cite as

Neuron specific enolase: a promising therapeutic target in acute spinal cord injury

  • Azizul Haque
  • Swapan K. Ray
  • April Cox
  • Naren L. Banik
Review Article


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.


Neuron specific enolase (NSE) Plasmin Matrix metalloproteinase (MMP) Major histocompatibility complex (MHC) Inflammation Neuronal death Spinal cord injury (SCI) 



This work was supported by grants from the South Carolina Spinal Cord Injury Research Fund (SCIRF 2015 P-01), National Institutes of Health (R01 CA129560 and R01 CA129560-S1), and MUSC Center for Global Health Faculty Pilot Program to A. Haque.

Compliance with ethical standards


The authors have no financial conflict of interest.


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Copyright information

© Springer Science+Business Media New York 2016

Authors and Affiliations

  • Azizul Haque
    • 1
  • Swapan K. Ray
    • 2
  • April Cox
    • 3
  • Naren L. Banik
    • 3
    • 4
  1. 1.Department of Microbiology and Immunology, Hollings Cancer CenterMedical University of South CarolinaCharlestonUSA
  2. 2.Department of Pathology, Microbiology, and ImmunologyUniversity of South Carolina School of MedicineColumbiaUSA
  3. 3.Department of NeurosurgeryMedical University of South CarolinaCharlestonUSA
  4. 4.Ralph H. Johnson Veterans Administration Medical CenterCharlestonUSA

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