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Polcyn et al. Neuroimmunol Neuroinflammation 2017;4:254-7 Neuroimmunology and
DOI: 10.20517/2347-8659.2017.59
Neuroinflammation

www.nnjournal.net
Editorial Open Access

Neuron specific enolase is a potential target

for regulating neuronal cell survival and

death: implications in neurodegeneration and

regeneration

Rachel Polcyn , Mollie Capone , Azim Hossain , Denise Matzelle , Naren L. Banik 1,2,3 , Azizul Haque 1
2,3
1
1
1,2
1 Department of Microbiology and Immunology, Hollings Cancer Center, Medical University of South Carolina, Charleston, SC 29425, USA.
2 Department of Neurosurgery, Medical University of South Carolina, Charleston, SC 29425, USA.
3 Ralph H. Johnson Veterans Administration Medical Center, Charleston, SC 29401, USA.
Correspondence to: Dr. Azizul Haque, Department of Microbiology and Immunology, Hollings Cancer Center, Medical University of South
Carolina, 173 Ashley Avenue, BSB-201, Charleston, SC 29425, USA. E-mail: haque@musc.edu
How to cite this article: Polcyn R, Capone M, Hossain A, Matzelle D, Banik NL, Haque A. Neuron specific enolase is a potential target for
regulating neuronal cell survival and death: implications in neurodegeneration and regeneration. Neuroimmunol Neuroinflammation 2017;4:254-7.

Article history: Received: 17 Nov 2017 Accepted: 17 Nov 2017 Published: 6 Dec 2017

Enolase is a multifunctional enzyme primarily involved especially cathepsins (e.g. Cathepsin X or Cat X), are
in catalyzing the conversion of 2-phosphoglycerate instrumental in processing several neuronal proteins
to phosphoenolpyruvate during glycolysis and the that generate either harmful or neuroprotective
reverse reaction during gluconeogenesis [1-4] . Though functions. Cathepsins and a neutral protease, calpain,
typically expressed in the cytosol, enolase has been also have regulatory functions in antigen processing
shown to migrate to the cell surface upon inflammatory and presentation, thereby inducing immune responses
[3]
signal . It then enhances antigen presentation for that can have either detrimental or beneficial effects
the invasion of host cells via plasminogen binding on neuronal cells. This editorial discusses the
and subsequent plasmin activation, leading to relationships between neuron specific enolase (NSE)
degradation of the extracellular matrix. Cell surface and Cat X activity in neuronal cells with a special
expression of enolase, possibly due to an association focus on their implications for neurodegeneration and
with the urokinase-type plasminogen activator (uPA)/ neuroprotection.
uPA receptor complex, additionally induces the
production of reactive oxygen species, nitric oxide, Distinct dimeric isoforms of enolase are composed
and pro-inflammatory cytokines [tumor necrotic of non-covalently linked α, β, or γ subunits and are
factor (TNF)-α, interleukin (IL)-1β, interferon-γ, tissue-specific . During development, injury, or
[3]
and transforming growth factor-β] and chemokines disease, α-enolase (enolase 1, non-neuronal enolase,
[monocyte chemotactic protein 1 and macrophage ENO1), which is primarily found in adult tissue, can be
inflammator y protein (MIP) -1α] to augment converted to γ-enolase (enolase 2, NSE) in neurons
neurodegenerative response [3,5] . Lysosomal proteases, and neuroendocrine cells. Similarly, α-enolase is

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