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Urokinase-type plasminogen activator is a modulator of synaptic plasticity in the central nervous system:implications for neurorepair in the ischemic brain

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Neural Regeneration Research 2020年第4期15卷 620-624页

作者： Manuel Yepes Division of Neuropharmacology and Neurologic Diseases Yerkes National Primate Research Center Department of Neurology Emory University School of Medicine Department of Neurology Veterans Affairs Medical Center

The last two decades have witnessed a rapid decrease in mortality due to acute cerebral ischemia that paradoxically has led to a rapid increase in the number of patients that survive an acute ischemic stroke with various degrees of disability.Unfortunately,the lack of an effective therapeutic strategy to promote neurological recovery among stroke survivors has led to a rapidly growing population of disabled patients.Thus,understanding the mechanisms of neurorepair in the ischemic brain is a priority with wide scientific,social and economic implications.Cerebral ischemia has a harmful effect on synaptic structure associated with the development of functional impairment.In agreement with these observations,experimental evidence indicates that synaptic repair underlies the recovery of neurological function following an ischemic stroke.Furthermore,it has become evident that synaptic plasticity is crucial not only during development and learning,but also for synaptic repair after an ischemic insult.The plasminogen activating system is assembled by a cascade of enzymes and their inhibitors initially thought to be solely involved in the generation of plasmin.However,recent work has shown that in the brain this system has an important function regulating the development of synaptic plasticity via mechanisms that not always require plasmin generation.Urokinase-type plasminogen activator(uPA)is a serine proteinase and one of the plasminogen activators,that upon binding to its receptor(uPAR)not only catalyzes the conversion of plasminogen into plasmin on the cell surface,but also activates cell signaling pathways that promote cell migration,proliferation and survival.The role of uPA is the brain is not fully understood.However,it has been reported while uPA and uPAR are abundantly found in the developing central nervous system,in the mature brain their expression is restricted to a limited group of cells.Remarkably,following an ischemic injury to the mature brain the expression of uPA and uPAR increases to levels comparable

关键词： cerebral ischemia neurorepair plasminogen plasticity stoke synapse urokinase urokinase receptor

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Hypoxia inducible factor-1 alpha stabilization for regenerative therapy in traumatic brain injury

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Neural Regeneration Research 2017年第5期12卷 696-701页

作者： Mushfiquddin Khan Hamza Khan Inderjit Singh Avtar K.Singh Department of Pediatrics Medical University of South Carolina Charleston SC USA College of Medicine University of South Carolina Columbia SC USA Department of Pathology and Laboratory Medicine Medical University of South Carolina Charleston SC USA Ralph H. Johnson VA Medical Center Charleston SC USA

Mild traumatic brain injury（TBI）, also called concussion, initiates sequelae leading to motor deficits, cognitive impairments and subtly compromised neurobehaviors. While the acute phase of TBI is associated with neuroinflammation and nitroxidative burst, the chronic phase shows a lack of stimulation of the neurorepair process and regeneration. The deficiency of nitric oxide（NO）, the consequent disturbed NO metabolome, and imbalanced mechanisms of S-nitrosylation are implicated in blocking the mechanisms of neurorepair processes and functional recovery in the both phases. Hypoxia inducible factor-1 alpha（HIF-1α）, a master regulator of hypoxia/ischemia, stimulates the process of neurorepair and thus aids in functional recovery after brain trauma. The activity of HIF-1α is regulated by NO via the mechanism of S-nitrosylation of HIF-1α. S-nitrosylation is dynamically regulated by NO metabolites such as S-nitrosoglutathione（GSNO） and peroxynitrite. GSNO stabilizes, and peroxynitrite destabilizes HIF-1α. Exogenously administered GSNO was found not only to stabilize HIF-1α and to induce HIF-1α-dependent genes but also to stimulate the regeneration process and to aid in functional recovery in TBI animals.

关键词： traumatic brain injury hypoxia inducible factor-1 alpha S-nitrosoglutathione neurorepair functional recovery

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Endothelial progenitor cells as a therapeutic option in intracerebral hemorrhage

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Neural Regeneration Research 2017年第4期12卷 558-561页

作者： Juan Pías-Peleteiro Francisco Campos José Castillo Tomás Sobrino Clinical Neurosciences Research Laboratory Department of NeurologyStroke UnitUniversity Clinical HospitalUniversidade de Santiago de CompostelaHealth Research Institute of Santiago de Compostela (IDIS)

Intracerebral hemorrhage （ICH） is the most severe cerebrovascular disease, which represents a leading cause of death and disability in developed countries. However, therapeutic options are limited, so is mandatory to investigate repairing processes after stroke in order to develop new therapeutic strategies able to promote brain repair processes. Therapeutic angiogenesis and vasculogenesis hold promise to improve outcome of ICH patients. In this regard, circulating endothelial progenitor cells （EPCs） have recently been suggested to be a marker of vascular risk and endothelial function. Moreover, EPC levels have been associated with good neurological and functional outcome as well as reduced residual hematoma volume in ICH patients. Finally, experimental and clinical studies indicate that EPC might mediate endothelial cell regeneration and neovascularization. Therefore, EPC-based therapy could be an excellent therapeutic option in ICH. In this mini-review, we discuss the present status of knowledge about the possible therapeutic role of EPCs in ICH, molecular mechanisms, and the future perspectives and strategies for their use in clinical practice.

关键词： cellular therapy endothelial progenitor cells growth factors intracerebral hemorrhage neurorepair outcome

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CNB-001 reduces paraplegia in rabbits following spinal cord ischemia

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Neural Regeneration Research 2019年第12期14卷 2192-2198页

作者： Paul A. Lapchak Paul D. Boitano Rene Bombien Daisy Chou Margot Knight Anja Muehle Mihaela Te Winkel Ali Khoynezhad Neurocore LLC Pomona CA USA Department of Surgery Memorial Care Health System Long Beach CA USA

aortic aneurysm repair and thoracic endovascular aortic repair results in devastating clinical deficits in patients. Because spinal cord ischemia is inadequately treated, we studied the effects of [4-((1E)-2-(5-(4-hydroxy-3-methoxystyryl-)-1-phenyl-1H-pyrazoyl-3-yl) vinyl)-2-methoxy-phenol)](CNB-001), a novel curcumin-based compound, in a rabbit SCI model. CNB-001 is known to inhibit human 5-lipoxygenase and 15-lipoxygenase and reduce the ischemia-induced inflammatory response. Moreover, CNB- 001 can reduce the level of oxidative stress markers and potentiate brain-derived neurotrophic factor and brain-derived neurotrophic factor receptor signaling. The Tarlov scale and quantal analysis technique results revealed that CNB-001 administered as an intravenous dose (bolus) 30 minutes prior to spinal cord ischemia improved the behaviors of female New Zealand White rabbits. The improvements were similar to those produced by the uncompetitive N-methyl-D-aspartate receptor antagonist memantine. At 48 hours after aortic occlusion, there was a 42.7% increase (P < 0.05) in tolerated ischemia duration (n = 14) for rabbits treated with CNB-001 (n = 16), and a 72.3% increase for rabbits treated with the positive control memantine (P < 0.05)(n = 23) compared to vehicle-treated ischemic rabbits (n = 22). CNB-001 is a potential important novel treatment for spinal cord ischemia induced by aortic occlusion. All experiments were approved by the CSMC Institutional Animal Care and Use Committee (IACUC #4311) on November 1, 2012.

关键词： curcumin analog spinal cord injury spinal cord ischemia thoraco-abdominal aortic aneurysm thoracic endovascular aortic repair motor function neuroprotection neurorepair

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Collagen for brain repair:therapeutic perspectives

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Neural Regeneration Research 2018年第4期13卷 595-598页

作者： Buket Ucar Christian Humpel Laboratory of Psychiatry and Experimental Alzheimer's Research Medical University of Innsbruck

Biomaterials have increasingly become a focus of research on neuroprotection and neuroregeneration.Collagen,in terms of brain repair,presents many advantages such as being remarkably biocompatible,biodegradable,versatile and non-toxic.Collagen can be used to form injectable scaffolds and micro/nano spheres in order to：（i） locally release therapeutic factors with the aim of protecting degenerating neurons in neurodegenerative conditions such as Alzheimer＇s or Parkinson＇s diseases,（ii） encapsulate stem cells for safe delivery,（iii） encapsulate genetically modified cells to provide a long term source of trophic factors,（iv） fill in the voids from injury to serve as a structural support and provide a permissive microenvironment to promote axonal growth.This mini-review summarizes different applications of collagen biomaterial for central nervous system protection and repair,as well as the future perspectives.Overall,collagen is a promising natural biomaterial with various applications which has the potential to progress the development of therapeutic strategies in central nervous system injuries and degeneration.

关键词： biomaterial collagen scaffold microspheres neuroprotection neuroregeneration neurorepair Alzheimer’s disease Parkinson’s disease

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The potential of a combined cell-based therapy and rehabilitation approach for stroke recovery

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Neuroprotection 2023年第2期1卷 117-129页

作者： Abdulhameed Bakreen Jukka Jolkkonen Department of Neurology University ofEastern FinlandKuopioFinland A.I.Virtanen Institute for Molecular Sciences University of Eastern FinlandKuopioFinland

Activation of neuroprotective and particularly later neurorestorative mechanisms after stroke attempts to restore or compensate for lost functions.This potentially opens a wide window for restorative therapies to promote brain repair and improve long-term functional recovery.Although extensively demonstrated in the preclinical setting,the efficacy of cell-based therapies in stroke patients has been modest at best,if any at all.Translational failure may be due to the ineffective survival and integration of transplanted cells in pro-death stroke microenvironments that are not conducive for the structural reconstruction of damaged brain tissue and repair-related network reorganization.Optimal systemic delivery,timing,cell product,and dose remain open as well.Fortunately,a better understanding of the brain plasticity mechanisms underlying stroke recovery has ushered in a combination approach of cell-based therapy and rehabilitation that is aimed at achieving additive,synergistic,or even maximal beneficial effects.This novel combination therapy is not only targeted at promoting exogenous and endogenous cell survival and augmenting stand-alone restorative mechanisms but also at utilizing rehabilitation to facilitate a graft–host structural and functional integration and plasticity that would effectively remodel stroke tissue and restitute lost functions.This review presents an overview of the combination of cell-based therapy and experimental rehabilitation in stroke models.It also discusses associated shortcomings as well as proposes strategies to address them and help facilitate the advancement of this combination approach.

关键词： brain regeneration cell-based therapy combination therapy neuroprotection neurorepair rehabilitation stroke

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