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Skeletal muscle as a molecular and cellular biomarker of disease progression in amyotrophic lateral sclerosis:a narrative review

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Neural Regeneration Research 2024年第4期19卷 747-753页

作者： Peter h.King Department of Neurology and center for Neurodegeneration and Experimental Therapeutics The University of Alabama at BirminghamBirminghamALUSA Birmingham veterans Affairs medical center BirminghamALUSA

Amyotrophic lateral sclerosis is a fatal multisystemic neurodegenerative disease with motor neurons being a primary target.Although progressive weakness is a hallmark feature of amyotrophic lateral sclerosis,there is considerable heterogeneity,including clinical presentation,progression,and the underlying triggers for disease initiation.Based on longitudinal studies with families harboring amyotrophic lateral sclerosis-associated gene mutations,it has become apparent that overt disease is preceded by a prodromal phase,possibly in years,where compensatory mechanisms delay symptom onset.Since 85-90%of amyotrophic lateral sclerosis is sporadic,there is a strong need for identifying biomarkers that can detect this prodromal phase as motor neurons have limited capacity for regeneration.Current Food and Drug administration-approved therapies work by slowing the degenerative process and are most effective early in the disease.Skeletal muscle,including the neuromuscular junction,manifests abnormalities at the earliest stages of the disease,before motor neuron loss,making it a promising source for identifying biomarkers of the prodromal phase.The accessibility of muscle through biopsy provides a lens into the distal motor system at earlier stages and in real time.The advent of“omics”technology has led to the identification of numerous dysregulated molecules in amyotrophic lateral sclerosis muscle,ranging from coding and non-coding RNAs to proteins and metabolites.This technology has opened the door for identifying biomarkers of disease activity and providing insight into disease mechanisms.A major challenge is correlating the myriad of dysregulated molecules with clinical or histological progression and understanding their relevance to presymptomatic phases of disease.There are two major goals of this review.The first is to summarize some of the biomarkers identified in human amyotrophic lateral sclerosis muscle that have a clinicopathological correlation with disease activity,evidence of a similar dysregulation in the SO

关键词： amyotrophic lateral sclerosis biomarkers clinicopathological correlation disease progression muscle biomarkers neurogenic atrophy neuromuscular junction non-coding RNAs presymptomatic stages skeletal muscle SOD1G93A mouse model

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

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Neural Regeneration Research 2023年第7期18卷 1457-1462页

作者： hannah MMcCoy Rachel Polcyn Naren LBanik Azizul haque Department of Microbiology and Immunology Medical University of South CarolinaCharlestonSCUSA Department of Neurosurgery Medical University of South CarolinaCharlestonSCUSA ralph h.johnson veterans administration medical center CharlestonSCUSA

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 discus

关键词： 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

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Clemastine in remyelination and protection of neurons and skeletal muscle after spinal cord injury

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Neural Regeneration Research 2023年第5期18卷 940-946页

作者： Ali Myatich Azizul haque Christopher Sole Naren L.Banik Department of Microbiology and Immunology Medical University of South CarolinaCharlestonSCUSA Department of Neurosurgery Medical University of South CarolinaCharlestonSCUSA ralph h.johnson veterans administration medical center CharlestonSCUSA Department of health and human Performance The CitadelCharlestonSCUSA

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.

关键词： axonal damage clemastine myelination neuronal death oligodendrocytes skeletal muscle spinal cord injury

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Neuroprotective effects of Alda-1 mitigate spinal cord injury in mice:involvement of Alda-1-induced ALDh2 activation-mediated suppression of reactive aldehyde mechanisms

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Neural Regeneration Research 2022年第1期17卷 185-193页

作者： Mushfiquddin Khan Fei Qiao Pavan Kumar S.M.Touhidul Islam Avtar K.Singh Jeseong Won Inderjit Singh Department of Pediatrics Medical University of South CarolinaCharlestonSCUSA Department of Pathology and Laboratory Medicine Medical University of South CarolinaCharlestonSCUSA ralph h.johnson VA medical center CharlestonSCUSA

Spinal cord injury(SCI)is associated with high production and excessive accumulation of pathological 4-hydroxy-trans-2-nonenal(4-hNE),a reactive aldehyde,formed by SCI-induced metabolic dysregulation of membrane lipids.Reactive aldehyde load causes redox alteration,neuroinflammation,neurodegeneration,pain-like behaviors,and locomotion deficits.Pharmacological scavenging of reactive aldehydes results in limited improved motor and sensory functions.In this study,we targeted the activity of mitochondrial enzyme aldehyde dehydrogenase 2(ALDh2)to detoxify 4-hNE for accelerated functional recovery and improved pain-like behavior in a male mouse model of contusion SCI.N-(1,3-benzodioxol-5-ylmethyl)-2,6-dichlorobenzamide(Alda-1),a selective activator of ALDh2,was used as a therapeutic tool to suppress the 4-hNE load.SCI was induced by an impactor at the T9–10 vertebral level.Injured animals were initially treated with Alda-1 at 2 hours after injury,followed by once-daily treatment with Alda-1 for 30 consecutive days.Locomotor function was evaluated by the Basso Mouse Scale,and pain-like behaviors were assessed by mechanical allodynia and thermal algesia.ALDh2 activity was measured by enzymatic assay.4-hNE protein adducts and enzyme/protein expression levels were determined by western blot analysis and histology/immunohistochemistry.SCI resulted in a sustained and prolonged overload of 4-hNE,which parallels with the decreased activity of ALDh2 and low functional recovery.Alda-1 treatment of SCI decreased 4-hNE load and enhanced the activity of ALDh2 in both the acute and the chronic phases of SCI.Furthermore,the treatment with Alda-1 reduced neuroinflammation,oxidative stress,and neuronal loss and increased adenosine 5′-triphosphate levels stimulated the neurorepair process and improved locomotor and sensory functions.Conclusively,the results provide evidence that enhancing the ALDh2 activity by Alda-1 treatment of SCI mice suppresses the 4-hNE load that attenuates neuroinflammation and neurodegeneration,promotes the neur

关键词： 4-hydroxy-trans-2-nonenal Alda-1 ALDh2 Basso Mouse Scale score functional recovery mitochondrial function neuroinflammation neuroprotection pain spinal cord injury

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Implications of enolase in the RANKL-mediated osteoclast activity following spinal cord injury

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BIOCELL 2021年第6期45卷 1453-1457页

作者： RAMShA ShAMS NAREN LBANIK AZIZUL hAQUE Department of Microbiology and Immunology Medical University of South CarolinaCharlestonSC 29425USA Department of Neurosurgery Medical University of South CarolinaCharlestonSC 29425USA ralph h.johnson veterans administration medical center CharlestonSC 29401USA

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.

关键词： Enolase RANK RANKL Osteoporosis Neuronal death Spinal cord injury

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hematopoietic stem cell-derived adipocytes and fibroblasts in the tumor microenvironment

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World Journal of Stem Cells 2015年第2期7卷 253-265页

作者： Ying Xiong Lindsay T Mc Donald Dayvia L Russell Ryan R Kelly Katie R Wilson Meenal Mehrotra Adam C Soloff Amanda C LaRue Research Services Ralph H Johnson Veterans Affairs Medical Center Department of Pathology and Laboratory Medicine Ralph H Johnson Veterans Affairs Medical Center the hollings Cancer center Medical University of South CarolinaRalph H Johnson Veterans Affairs Medical Center Department of Microbiology and Immunology Ralph H Johnson Veterans Affairs Medical Center

The tumor microenvironment(TME) is complex and constantly evolving. This is due, in part, to the crosstalk between tumor cells and the multiple cell types that comprise the TME, which results in a heterogeneous population of tumor cells and TME cells. This review will focus on two stromal cell types, the cancerassociated adipocyte(CAA) and the cancer-associated fibroblast(CAF). In the clinic, the presence of CAAs and CAFs in the TME translates to poor prognosis in multiple tumor types. CAAs and CAFs have an activated phenotype and produce growth factors, inflammatory factors, cytokines, chemokines, extracellular matrix components, and proteases in an accelerated and aberrant fashion. Through this activated state, CAAs and CAFs remodel the TME, thereby driving all aspects of tumor progression, including tumor growth and survival, chemoresistance, tumor vascularization, tumor invasion, and tumor cell metastasis. Similarities in the tumorpromoting functions of CAAs and CAFs suggest that a multipronged therapeutic approach may be necessary to achieve maximal impact on disease. While CAAs and CAFs are thought to arise from tissues adjacent to the tumor, multiple alternative origins for CAAs and CAFs have recently been identified. Recent studies from our lab and others suggest that the hematopoietic stem cell, through the myeloid lineage, may serve as a progenitor for CAAs and CAFs. We hypothesize that the multiple origins of CAAs and CAFs may contribute to the heterogeneity seen in the TME. Thus, a better understanding of the origin of CAAs and CAFs, how this origin impacts their functions in the TME, and thetemporal participation of uniquely originating TME cells may lead to novel or improved anti-tumor therapeutics.

关键词： hematopoietic stem cell Cancer associatedadipocyte Mesenchymal stromal cell Tumor progression Cancer associated fibroblast Plasticity Metastasis Fibrocyte

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Future directions for using estrogen receptor agonists in the treatment of acute and chronic spinal cord injury

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Neural Regeneration Research 2016年第9期11卷 1418-1419页

作者： Swapan K. Ray Supriti Samntaray Naren L. Banik Department of Pathology Microbiology and Immunology University of South Carolina School of Medicine Columbia SC USA Department of Neurosciences Medical University of South Carolina Charleston SC USA Department of Neurology and Neurosurgery Medical University of South Carolina Charleston SC USA ralph h. johnson veterans administration medical center Charleston SC USA

All synthetic and natural estrogen receptor agonists, in- cluding the most potent physiological molecule estrogen or estradiol （E2）, work typically via activation of nuclear estrogen receptor alpha （ERα） and estrogen receptor beta （ERβ）. Both ERα and ERβ modulate the expression of a variety of genes in the cells. Neurons and glial cells express ERa and ERβ. Many studies so far from our and other laboratories have firmly established the mode of actions that ERα and ERβ agonists are very promising anti-inflammatory and neuroprotective agents in the treatment of neurodegenera- rive diseases and injuries including spinal cord injury （SCI）（Chakrabarti et al., 2014a）.

关键词： Future directions for using estrogen receptor agonists in the treatment of acute and chronic spinal cord injury SCI

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Neuron-to-vessel signaling is a required feature of aberrant stem cell commitment after soft tissue trauma

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Bone Research 2022年第3期10卷 615-626页

作者： Qizhi Qin Mario Gomez-Salazar Masnsen Cherief Chase A.Pagani Seungyong Lee Charles hwang Robert J.Tower Sharon Onggo Yuxiao Sun Abhinav Piplani Zhao Li Sowmya Ramesh Thomas L.Clemens Benjamin Levi Aaron W.James Department of Pathology Johns Hopkins UniversityBaltimoreMD 21205USA center for Organogenesis and Trauma Department of SurgeryUniversity of TexasSouthwesternTXUSA Department of Plastic Surgery HarvardCambridgeMA 02138USA Department of Orthopaedics Johns Hopkins UniversityBaltimoreMD 21205USA Baltimore veterans administration medical center BaltimoreMD 21201USA

The functional interdependence of nerves and blood vessels is a well-established concept during tissue morphogenesis, yet the role of neurovascular coupling in proper and aberrant tissue repair is an emerging field of interest. here, we sought to define the regulatory relationship of peripheral nerves on vasculature in a severe extremity trauma model in mice, which results in aberrant cell fate and heterotopic ossification(hO). First, a high spatial degree of neurovascular congruency was observed to exist within extremity injury associated heterotopic ossification. Vascular and perivascular cells demonstrate characteristic responses to injury,as assessed by single cell RNA sequencing. This vascular response to injury was blunted in neurectomized mice, including a decrease in endothelial proliferation and type h vessel formation, and a downregulation of key transcriptional networks associated with angiogenesis. Independent mechanisms to chemically or genetically inhibit axonal ingrowth led to similar deficits in hO site angiogenesis, a reduction in type h vessels, and heterotopic bone formation. Finally, a combination of single cell transcriptomic approaches within the dorsal root ganglia identified key neural-derived angiogenic paracrine factors that may mediate neuron-to-vascular signaling in hO. These data provide further understanding of nerve-to-vessel crosstalk in traumatized soft tissues, which may reflect a key determinant of mesenchymal progenitor cell fate after injury.

关键词： aberrant trauma nerves

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Neuron specific enolase is a potential target for regulating neuronal cell survival and death: implications in neurodegeneration and regeneration

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Neuroimmunology and Neuroinflammation 2017年第12期4卷 254-257页

作者： Rachel Polcyn Mollie Capone Azim hossain Denise Matzelle Naren L.Banik Azizul haque Department of Microbiology and Immunology Hollings Cancer CenterMedical University of South CarolinaCharlestonSC 29425USA Department of Neurosurgery Medical University of South CarolinaCharlestonSC 29425USA ralph h.johnson veterans administration medical center CharlestonSC 29401USA.

Enolase is a multifunctional enzyme primarily involved in catalyzing the conversion of 2-phosphoglycerate to phosphoenolpyruvate during glycolysis and the reverse reaction during gluconeogenesis[1-4].Though typically ... 详细信息

关键词： Neuron specific enolase potential target regulating neuronal cell survival

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MRI analysis and clinical significance of lower extremity muscle cross-sectional area after spinal cord injury

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Neural Regeneration Research 2017年第5期12卷 714-722页

作者： Robert M.Lester Kori johnson Refka E.Khalil Rehan Khan Ashraf S.Gorgey Spinal Cord Injury and Disorders center Hunter Holmes McGuire Veterans Administration Medical Center (VAMC) Richmond VA USA Department of Physical Medicine and Rehabilitation Virginia Commonwealth University Richmond VA USA Radiology Service Hunter Holmes McGuire Veterans Administration Medical Center (VAMC) Richmond VA USA

Shortly after spinal cord injury（SCI）, the musculoskeletal system undergoes detrimental changes in size and composition, predominantly below the level of injury. The loss of muscle size and strength, along with increased immobility, predisposes persons with SCI to rapid and severe loss in bone mineral density and other health related consequences. Previous studies have highlighted the significance of measuring thigh muscle cross-sectional area, however, measuring the size and composition of muscles of the lower leg may provide insights on how to decrease the risk of various comorbidities. The purpose of the current review was to summarize the methodological approach to manually trace and measure the muscles of the lower leg in individuals with SCI, using magnetic resonance imaging. We also intend to highlight the significance of analyzing lower leg muscle cross-sectional area and its relationship to musculoskeletal and vascular systems in persons with SCI.

关键词： spinal cord injury magnetic resonance imaging pressure ulcers venous thromboembolism cardiovascular disease bone health

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