دورية أكاديمية

Regulation of enolase activation to promote neural protection and regeneration in spinal cord injury

التفاصيل البيبلوغرافية
العنوان: Regulation of enolase activation to promote neural protection and regeneration in spinal cord injury
المؤلفون: Hannah M McCoy, Rachel Polcyn, Naren L Banik, Azizul Haque
المصدر: Neural Regeneration Research, Vol 18, Iss 7, Pp 1457-1462 (2023)
بيانات النشر: Wolters Kluwer Medknow Publications, 2023.
سنة النشر: 2023
المجموعة: LCC:Neurology. Diseases of the nervous system
مصطلحات موضوعية: cathepsin x, enoblock, enolase, glia, mitogen-activated protein kinase/extracellular signal-regulated kinase, neurodegeneration, neuroinflammation, phosphatidylinositol-4, 5-bisphosphate 3-kinase/protein kinase b, rho-associated protein kinase, spinal cord injury, Neurology. Diseases of the nervous system, RC346-429
الوصف: Spinal cord injury (SCI) is a debilitating condition characterized by damage to the spinal cord resulting in loss of function, mobility, and sensation with no U.S. Food and Drug Administration-approved cure. Enolase, a multifunctional glycolytic enzyme upregulated after SCI, promotes pro- and anti-inflammatory events and regulates functional recovery in SCI. Enolase is normally expressed in the cytosol, but the expression is upregulated at the cell surface following cellular injury, promoting glial cell activation and signal transduction pathway activation. SCI-induced microglia activation triggers pro-inflammatory mediators at the injury site, activating other immune cells and metabolic events, i.e., Rho-associated kinase, contributing to the neuroinflammation found in SCI. Enolase surface expression also activates cathepsin X, resulting in cleavage of the C-terminal end of neuron-specific enolase (NSE) and non-neuronal enolase (NNE). Fully functional enolase is necessary as NSE/NNE C-terminal proteins activate many neurotrophic processes, i.e., the plasminogen activation system, phosphatidylinositol-4,5-bisphosphate 3-kinase/protein kinase B, and mitogen-activated protein kinase/extracellular signal-regulated kinase. Studies here suggest an enolase inhibitor, ENOblock, attenuates the activation of Rho-associated kinase, which may decrease glial cell activation and promote functional recovery following SCI. Also, ENOblock inhibits cathepsin X, which may help prevent the cleavage of the neurotrophic C-terminal protein allowing full plasminogen activation and phosphatidylinositol-4,5-bisphosphate 3-kinase/mitogen-activated protein kinase activity. The combined NSE/cathepsin X inhibition may serve as a potential therapeutic strategy for preventing neuroinflammation/degeneration and promoting neural cell regeneration and recovery following SCI. The role of cell membrane-expressed enolase and associated metabolic events should be investigated to determine if the same strategies can be applied to other neurodegenerative diseases. Hence, this review discusses the importance of enolase activation and inhibition as a potential therapeutic target following SCI to promote neuronal survival and regeneration.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1673-5374
Relation: http://www.nrronline.org/article.asp?issn=1673-5374;year=2023;volume=18;issue=7;spage=1457;epage=1462;aulast=McCoy; https://doaj.org/toc/1673-5374
DOI: 10.4103/1673-5374.361539
URL الوصول: https://doaj.org/article/c3aabf5723a84655a7553989df5fba22
رقم الأكسشن: edsdoj.3aabf5723a84655a7553989df5fba22
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:16735374
DOI:10.4103/1673-5374.361539