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Neuroprotective role of Noggin in spinal cord injury

Neural Regeneration Research 2023年第3期18卷 492-496页

作者： Nadia Al-Sammarraie Mohammed Mahmood swapan k.ray Department of Pathology Microbiologyand ImmunologyUniversity of South Carolina School of MedicineColumbiaSCUSA

Spinal cord injury is one of the leading causes of morbidity and mortality among young adults in many countries including the United States.Difficulty in the regeneration of neurons is one of the main obstacles that leave spinal cord injury patients with permanent paralysis in most instances.Recent research has found that preventing acute and subacute secondary cellular damages to the neurons and supporting glial cells can help slow the progression of spinal cord injury pathogenesis,in part by reactivating endogenous regenerative proteins including Noggin that are normally present during spinal cord development.Noggin is a complex protein and natural inhibitor of the multifunctional bone morphogenetic proteins,and its expression is high during spinal cord development and after induction of spinal cord injury.In this review article,we first discuss the change in expression of Noggin during pathogenesis in spinal cord injury.Second,we discuss the current research knowledge about the neuroprotective role of Noggin in preclinical models of spinal cord injury.Lastly,we explain the gap in the knowledge for the use of Noggin in the treatment of spinal cord injury.The results from extensive in vitro and in vivo research have revealed that the therapeutic efficacy of Noggin treatment remains debatable due to its neuroprotective effects observed only in early phases of spinal cord injury but little to no effect on altering pathogenesis and functional recovery observed in the chronic phase of spinal cord injury.Furthermore,clinical information regarding the role of Noggin in the alleviation of progression of pathogenesis,its therapeutic efficacy,bioavailability,and safety in human spinal cord injury is still lacking and therefore needs further investigation.

关键词： apoptosis astrocyte differentiation axon myelination axon regeneration bone morphogenetic protein glial scar heterotrophic ossification neurogenesis neuropathic pain Noggin spinal cord injury

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Modulation of autophagy for neuroprotection and functional recovery in traumatic spinal cord injury

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Neural Regeneration Research 2020年第9期15卷 1601-1612页

作者： swapan k.ray Department of Pathology Microbiology and Immunology University of South Carolina School of Medicine

Spinal cord injury(SCI) is a serious central nervous system trauma that leads to loss of motor and sensory functions in the SCI patients. One of the cell death mechanisms is autophagy, which is ‘self-eating' of the damaged and misfolded proteins and nucleic acids, damaged mitochondria, and other impaired organelles for recycling of cellular building blocks. Autophagy is different from all other cell death mechanisms in one important aspect that it gives the cells an opportunity to survive or demise depending on the circumstances. Autophagy is a therapeutic target for alleviation of pathogenesis in traumatic SCI. However, functions of autophagy in traumatic SCI remain controversial. Spatial and temporal patterns of activation of autophagy after traumatic SCI have been reported to be contradictory. Formation of autophagosomes following therapeutic activation or inhibition of autophagy flux is ambiguous in traumatic SCI studies. Both beneficial and harmful outcomes due to enhancement autophagy have been reported in traumatic SCI studies in preclinical models. Only further studies will make it clear whether therapeutic activation or inhibition of autophagy is beneficial in overall outcomes in preclinical models of traumatic SCI. Therapeutic enhancement of autophagy flux may digest the damaged components of the central nervous system cells for recycling and thereby facilitating functional recovery. Many studies demonstrated activation of autophagy flux and inhibition of apoptosis for neuroprotective effects in traumatic SCI. Therapeutic induction of autophagy in traumatic SCI promotes axonal regeneration, supporting another beneficial role of autophagy in traumatic SCI. In contrast, some other studies demonstrated that disruption of autophagy flux in traumatic SCI strongly correlated with neuronal death at remote location and impaired functional recovery. This article describes our current understanding of roles of autophagy in acute and chronic traumatic SCI, crosstalk between autophagy and apoptosis, therapeutic act

关键词： apoptosis autophagy autophagy modulation neuroprotection traumatic spinal cord injury

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Bone morphogenic protein signaling in spinal cord injury

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Neuroimmunology and Neuroinflammation 2021年第1期8卷 53-63页

作者： Nadia Al-Sammarraie swapan k.ray Department of Pathology Microbiologyand ImmunologyUniversity of South Carolina School of MedicineColumbiaSC 29209USA

Spinal cord injury(SCI)is a debilitating injury that results from traumatic or non-traumatic insults to the spinal cord,causing significant impairment of the patient's activity and quality of life.Bone morphogenic proteins(BMPs)are a group of polyfunctional cytokines belonging to the transforming growth factor beta superfamily that regulates a wide variety of cellular functions in healthy and disease states.Recent studies suggest that dysregulation of BMP signaling is involved in neuronal demyelination and death after traumatic SCI.The focus of this article is to describe our current understanding of the role of BMP signaling in the regulation of cell fate,proliferation,apoptosis,autophagy,and inflammation in traumatic SCI.First,we will describe the expression of BMPs and pattern of BMP signaling before and after traumatic SCI in rodent models and in vitro.Next,we will discuss the role of BMP in the regulation of neuronal and glial cell differentiation,survival,functional recovery from traumatic SCI,and the gap in knowledge in this area that requires further investigation to improve SCI prognosis.

关键词： Spinal cord injury bone morphogenic protein apoptosis proliferation autophagy differentiation inflammation

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Potential therapeutic roles of retinoids for prevention of neuroinflammation and neurodegeneration in Alzheimer’s disease

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Neural Regeneration Research 2019年第11期14卷 1880-1892页

作者： Bhaskar C. Das Somsankar Dasgupta swapan k. ray Department of Medicine Icahn School of Medicine at Mount SinaiNew YorkNYUSA Department of Neuroscience and Regenerative Medicine Institute of Molecular Medicine and GeneticsAugusta UniversityAugustaGAUSA Department of Pathology Microbiologyand ImmunologyUniversity of South Carolina School of MedicineColumbiaSCUSA

All retinoids, which can be natural and synthetic, are chemically related to vitamin A. Both natural and synthetic retinoids use specific nuclear receptors such as retinoic acid receptors and retinoid X receptors to activate specific signaling pathways in the cells. Retinoic acid signaling is extremely important in the central nervous system. Impairment of retinoic acid signaling pathways causes severe pathological processes in the central nervous system, especially in the adult brain. Retinoids have major roles in neural patterning, differentiation, axon outgrowth in normal development, and function of the brain. Impaired retinoic acid signaling results in neuroinflammation, oxidative stress, mitochondrial malfunction, and neurodegeneration leading to progressive Alzheimer’s disease, which is pathologically characterized by extra-neuronal accumulation of amyloid plaques(aggregated amyloid-beta) and intra-neurofibrillary tangles(hyperphosphorylated tau protein) in the temporal lobe of the brain. Alzheimer’s disease is the most common cause of dementia and loss of memory in old adults. Inactive cholinergic neurotransmission is responsible for cognitive deficits in Alzheimer’s disease patients. Deficiency or deprivation of retinoic acid in mice is associated with loss of spatial learning and memory. Retinoids inhibit expression of chemokines and neuroinflammatory cytokines in microglia and astrocytes, which are activated in Alzheimer’s disease. Stimulation of retinoic acid receptors and retinoid X receptors slows down accumulation of amyloids, reduces neurodegeneration, and thereby prevents pathogenesis of Alzheimer’s disease in mice. In this review, we described chemistry and biochemistry of some natural and synthetic retinoids and potentials of retinoids for prevention of neuroinflammation and neurodegeneration in Alzheimer’s disease.

关键词： Alzheimer's disease amyloid plaques neurofibrillary tangles neuroinflammation neurodegeneration retinoids

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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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Histone deacetylase enzymes and selective histone deacetylase inhibitors for antitumor effects and enhancement of antitumor immunity in glioblastoma

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Neuroimmunology and Neuroinflammation 2018年第11期5卷 1-18页

作者： Caleb J.Yelton swapan k.ray Department of Pathology Microbiologyand ImmunologyUniversity of South Carolina School of MedicineColumbiaSC 29209USA

Glioblastoma multiforme (GBM), which is the most common primary central nervous system malignancy in adults, has long presented a formidable challenge to researchers and clinicians alike. Dismal 5-year survival rates of the patients with these tumors and the ability of the recurrent tumors to evade primary treatment strategies have prompted a need for alternative therapies in the treatment of GBM. Histone deacetylase (HDAC) inhibitors are currently a potential epigenetic therapy modality under investigation for use in GBM with mixed results. While these agents show promise through a variety of proposed mechanisms in the pre-clinical realm, only several of these agents have shown this same promise when translated into the clinical arena, either as monotherapy or for use in combination regimens. This review will examine the current state of use of HDAC inhibitors in GBM, the mechanistic rationale for use of HDAC inhibitors in GBM, and then examine an exciting new mechanistic revelation of certain HDAC inhibitors that promote antitumor immunity in GBM. The details of this antitumor immunity will be discussed with an emphasis on application of this antitumor immunity towards developing alternative therapies for treatment of GBM. The final section of this article will provide an overview of the current state of immunotherapy targeted specifically to GBM.

关键词： Glioblastoma histone deacetylase inhibitors antitumor effects antitumor immunity

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Roles of miRNAs in spinal cord injury and potential therapeutic interventions

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Neuroimmunology and Neuroinflammation 2019年第10期6卷 1-11页

作者： Badria Almurshidi Wayne Carver Geoff Scott swapan k.ray Department of Environmental Health Sciences Arnold School of Public HealthCENRUniversity of South CarolinaColumbiaSC 29209USA Department of Cell Biology and Anatomy School of MedicineUniversity of South CarolinaColumbiaSC 29209USA Department of Pathology Microbiologyand ImmunologySchool of MedicineUniversity of South CarolinaColumbiaSC 29209USA

Spinal cord injury(SCI)affects approximately 200,000 individuals per year worldwide.There are more than 27 million people worldwide living with long-term disability due to SCI.Historically,it was thought that the central nervous system(CNS)had little ability for regeneration;however,more recent studies have demonstrated potential for repair within the CNS.Because of this,there exists a renewed interest in the discovery of novel approaches to promote regeneration in the CNS including the spinal cord.It is important to know the roles of the microRNAs(miRNAs)in modulation of pathogenesis in SCI and the potentials of the miRNA-based clinical interventions for controlling post-injury symptoms and improving functional recovery.The miRNAs,which are non-coding RNAs with an average of 22 nucleotides in length,are post-transcriptional gene regulators that cause degradation of the target mRNAs and thus negatively control their translation.This review article focuses on current research related to miRNAs and their roles in modulating SCI symptoms,asserting that miRNAs contribute to critical post-SCI molecular processes including neuroplasticity,functional recovery,astrogliosis,neuropathic pain,inflammation,and apoptosis.In particular,miR-96 provides a promising therapeutic opportunity to improve the outcomes of clinical interventions,including the way SCI injuries are evaluated and treated.

关键词： Spinal cord injury miRNAs astrogliosis neuropathic pain inflammation apoptosis functional recovery

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Economic impact of traumatic spinal cord injuries in the United States

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Neuroimmunology and Neuroinflammation 2019年第7期6卷 1-11页

作者： Christopher H.Merritt Matthew A.Taylor Caleb J.Yelton swapan k.ray Department of Pathology Microbiologyand ImmunologyUniversity of South Carolina School of MedicineColumbiaSC 29209USA

Individuals having sustained traumatic spinal cord injury(TSCI)in the United States are living longer as compared to historical trends,thanks to an ever-evolving understanding of the nature of this injury.Despite this,multiple barriers to care for TSCI patients remain including variations in government-issued veteran insurance,privatized insurance,and among uninsured individuals.The United States alone experiences 12,000 new TSCI cases every year,many of these are found to occur in a growing proportion of elderly individuals.It is crucial to understand both the short-term direct costs as wells as the long-term rehabilitation costs required by these TSCI patients.The lifetime financial burden for those having sustained a TSCI can be immense for patients,insurance companies,and hospital systems alike.Among those with TSCI,re-hospitalization rates are high,leading to increased healthcare resource utilization within this specific patient population.Costs can quickly balloon into hundreds of thousands of dollars and cause a profound financial burden for these patients.This review article seeks to communicate an understanding of the current financial landscape surrounding TSCI patients.The authors will also examine the costs of acute emergency room surgical care such as American spinal injury association grade,hospital length of stay,as well as the timing delay between injury and surgical decompression.Long-term costs associated with TSCI such as rehabilitation,care of secondary comorbidities,and post-injury employment prospects will be examined as well.These costs will be framed from the patient's perspective as well as from both the hospital and insurance company's perspectives.It is hoped a complete understanding as to what makes TSCI such a medically and financially burdensome injury will allow for improved healthcare resource utilization in this population.

关键词： Traumatic spinal cord injury healthcare resource American spinal injury association grade hospital length of stay rehabilitation post-injury employment

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EWS knockdown and Taxifolin Treatment Induced Differentiation and Removed DNA Methylation from p53 Promoter to Promote Expression of Puma and Noxa for Apoptosis in Ewing’s Sarcoma

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Journal of Cancer Therapy 2014年第12期5卷 1092-1113页

作者： Mohammad Motarab Hossain swapan kumar ray Department of Pathology Microbiology and Immunology University of South Carolina School of Medicine Columbia SC USA

Ewing’s sarcoma is a pediatric tumor that mainly occurs in soft tissues and bones. Malignant characteristics of Ewing’s sarcoma are correlated with expression of EWS oncogene. We achieved knockdown of EWS expression using a plasmid vector encoding EWS short hairpin RNA (shRNA) to increase anti-tumor mechanisms of taxifolin (TFL), a new flavonoid, in human Ewing’s sarcoma cells in culture and animal models. Immunofluorescence microscopy and flow cytometric analysis showed high expression of EWS in human Ewing’s sarcoma Sk-N-MC and RD-ES cell lines. EWS shRNA plus TFL inhibited 80% cell viability and caused the highest decreases in EWS expression at mRNA and protein levels in both cell lines. knockdown of EWS expression induced morphological features of differentiation. EWS shRNA plus TFL caused more alterations in molecular markers of differentiation than either agent alone. EWS shRNA plus TFL caused the highest decreases in cell migration with inhibition of survival, angiogenic and invasive factors. knockdown of EWS expression was associated with removal of DNA methylation from p53 promoter, promoting expression of p53, Puma, and Noxa. EWS shRNA plus TFL induced the highest amounts of apoptosis with activation of extrinsic and intrinsic pathways in both cell lines in culture. EWS shRNA plus TFL also inhibited growth of Ewing’s sarcoma tumors in animal models due to inhibition of differentiation inhibitors and angiogenic and invasive factors and also induction of activation of caspase-3 for apoptosis. Collectively, knockdown of EWS expression increased various anti-tumor mechanisms of TFL in human Ewing’s sarcoma in cell culture and animal models.

关键词： Apoptosis Differentiation Ewing’s Sarcoma EWS shRNA p53 Promoter Taxifolin

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Induction of Mitochondrial Pathways and Endoplasmic Reticulum Stress for Increasing Apoptosis in Ectopic and Orthotopic Neuroblastoma Xenografts

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Journal of Cancer Therapy 2011年第2期2卷 77-90页

作者： Surajit karmakar Subhasree Roy Choudhury Naren Lal Banik swapan kumar ray Department of Pathology Microbiology and Immunology University of South Carolina School of Medicine Columbia South Carolina USA.

Cancers are characterized by deregulation of multiple signaling pathways and thus monotherapies are hardly effective. Neuroblastoma, which often occurs in adrenal glands, is the most common childhood malignancy. Malignant neuroblastoma resists traditional treatments and further studies are needed for effective therapeutic interventions. We evaluated synergistic efficacy of N-(4-hydroxyphenyl) retinamide (4-HPR) and genistein (GST) for induction of apoptosis in human malignant neuroblastoma SH-SY5Y and Sk-N-BE2 cells in culture and activation of multiple pathways for increasing apoptosis in ectopic and orthotopic neuroblastoma xenografts in nude mice. Combination of 4-HPR and GST synergistically reduced cell viability, caused subG1 accumulation, increased caspase-3 activity for apoptosis in vitro and reduced tumor growth in vivo. Western blotting indicated that combination therapy down regulated Id2 to induce differentiation, increased pro-apoptotic Bax and decreased anti-apoptotic Bcl-2 leading to an increase in Bax:Bcl-2 ratio, increased mitochondrial Bax level, caused mitochondrial release of Smac/Diablo, down regulation of the baculovirus inhibitor-of-apoptosis repeat containing (BIRC) proteins such as BIRC-2 and BIRC-3, and activation of calpain and caspase-3 in SH-SY5Y xenografts. Accumulation of apoptosis-inducing-factor (AIF) in cytosol and increase in caspase-4 activation suggested involvement of mitochondrial pathway and endoplasmic reticulum (ER) stress, respectively, for apoptosis in SH-SY5Y xenografts. In situ immunofluorescent labelings of SH-SY5Y and Sk-N-BE2 xenograft sections showed overexpression of calpain, caspase-12, and caspase-3, and AIF, suggesting induction of mitochondrial caspase-dependent and caspase-independent pathways for apoptosis. Collectively, synergistic effects of 4-HPR and GST induced mitochondrial pathways and also ER stress for increasing apoptosis in ectopic and orthotopic neuroblastoma xenografts in nude mice.

关键词： Apoptosis Endoplasmic Reticulum Stress Genistein N-(4-Hydroxyphenyl) Retinamide Neuroblastoma

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