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| 1 | Regulation of enolase activation to promote neural protection and regeneration in spinal cord injury显示文摘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. | Hannah MMcCoy Rachel Polcyn Naren LBanik Azizul Haque | 2023 | Neural Regeneration Research2023，18，7： | 3 |
| 2 | Implications of enolase in the RANKL-mediated osteoclast activity following spinal cord injury显示文摘Spinal Cord Injury(SCI)is a debilitating condition characterized by damage to the spinal cord,resulting in loss of function,mobility,and sensation.Although increasingly prevalent in the US,no FDA-approved therapy exists due to the unfortunate complexity of the condition,and the difficulties of SCI may be furthered by the development of SCI-related complications,such as osteoporosis.SCI demonstrates two crucial stages for consideration:the primary stage and the secondary stage.While the primary stage is suggested to be immediate and irreversible,the secondary stage is proposed as a promising window of opportunity for therapeutic intervention.Enolase,a metabolic enzyme upregulated after SCI,performs non-glycolytic functions,promoting inflammatory events via extracellular degradative actions and increased production of inflammatory cytokines and chemokines.Neuron-specific enolase(NSE)serves as a biomarker of functional damage to neurons following SCI,and the inhibition of NSE has been demonstrated to reduce signs of secondary injury of SCI and to ameliorate dysfunction.This Viewpoint article involves enolase activation in the regulation of RANK-RANKL pathway and summarizes succinctly the mechanisms influencing osteoclast-mediated resorption of bone in SCI.Our laboratory proposes that inhibition of enolase activation may reduce SCI-induced inflammatory response and decrease osteoclast activity,limiting the chances of skeletal tissue loss in SCI. | RAMSHA SHAMS NAREN LBANIK AZIZUL HAQUE | 2021 | BIOCELL2021，45，6： | 3 |
| 3 | Clemastine in remyelination and protection of neurons and skeletal muscle after spinal cord injury显示文摘Spinal cord injuries affect nearly five to ten individuals per million every year. Spinal cord injury causes damage to the nerves, muscles, and the tissue surrounding the spinal cord. Depending on the severity, spinal injuries are linked to degeneration of axons and myelin, resulting in neuronal impairment and skeletal muscle weakness and atrophy. The protection of neurons and promotion of myelin regeneration during spinal cord injury is important for recovery of function following spinal cord injury. Current treatments have little to no effect on spinal cord injury and neurogenic muscle loss. Clemastine, an Food and Drug Administration-approved antihistamine drug, reduces inflammation, protects cells, promotes remyelination, and preserves myelin integrity. Recent clinical evidence suggests that clemastine can decrease the loss of axons after spinal cord injury, stimulating the differentiation of oligodendrocyte progenitor cells into mature oligodendrocytes that are capable of myelination. While clemastine can aid not only in the remyelination and preservation of myelin sheath integrity, it also protects neurons. However, its role in neurogenic muscle loss remains unclear. This review discusses the pathophysiology of spinal cord injury, and the role of clemastine in the protection of neurons, myelin, and axons as well as attenuation of skeletal muscle loss following spinal cord injury. | Ali Myatich Azizul Haque Christopher Sole Naren L.Banik | 2023 | Neural Regeneration Research2023，18，5： | 2 |
| 4 | Apoptosis in Toxoplasma gondii activated T cells: The role of IFNγ in enhanced alteration of Bcl-2 expression and mitochondrial membrane potential显示文摘 | Sakhina Begum-Haque Azizul Haque Lloyd H. Kasper | 2009 | Microbial Pathogenesis2009，，5： | 1 |
| 5 | Effect of mild alkali pretreatment on structural changes of reed (Phragmites communis Trinius) straw 显示文摘 | Dhirendra Nath Barman Md Azizul Haque Tae Ho Kang | 2014 | Environmental Technology2014，35，2： | 1 |
| 6 | Neurological nmnifestations of Puffer fish poisoning and it' s outcome: study of 83 cases显示文摘 | AZIZUL HAQUE M TARIKUL ISLAM Q RAZZAK M A | 2008 | Teach Assoc J2008，21，2： | 1 |
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