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| 1 | Down-Regulation of Neurocan Expression in Reactive Astrocytes Promotes Axonal Regeneration and Facilitates the Neurorestorative Effects of Bone Marrow Stromal Cells in the Ischemic Rat Brain显示文摘脑卒中后缺血组织边界形成胶质疤痕,抑制轴突再生。神经蛋白聚糖是一种轴突延长抑制分子,在卒中后胶质疤痕中表达上调。骨髓基质干细胞(BMSCs)可降低胶质疤痕壁的厚度,加速缺血周边区的轴突重塑。为了进一步明确BMSCs在轴突再生中的作用及机制,本文重点研究脑缺血组织中BMSCs对神经蛋白聚糖表达的作用。31只成年雄性Wistar大鼠大脑中动脉阻塞(MCAo)2 h,24 h后从中选择16只给予尾静脉注射3×106鼠BMSCs(BMSCs组),15只注射磷酸盐缓冲生理盐水(对照组)。缺血后8 d处死实验大鼠,免疫染色表明反应性星形胶质细胞是神经蛋白聚糖的原始来源,且BMSCs组缺血半暗带脑组织的神经聚糖表达明显低于对照组,生长相关蛋白43表达高于对照组,这在蛋白印迹分析中得到确认。为了进一步检测BMSCs在星形胶质细胞神经蛋白聚糖表达中的作用,用激光捕获显微切割法从缺血周边区收集单纯的反应性星形胶质细胞。BMSCs组的神经蛋白聚糖基因表达明显下调(n=4/组)。原代培养的星形胶质细胞也表现出相同改变,糖氧剥离的星形胶质细胞再给氧时与BMSCs共培养会抑制神经蛋白聚糖基因的表达上调(n=3/组)。本研究表明BMSCs通过下调梗死周边星形胶质细胞中神经蛋白聚糖的表达来促进轴突再生。 | LI HONG SHEN YI LI QI GAO SMITA SAVANT-BHONSALE AND MICHAEL CHOPP | 2008 | 神经损伤与功能重建2008，3，6： | 51 |
| 2 | Experimental animal models and infl ammatory cellular changes in cerebral ischemic and hemorrhagic stroke显示文摘Stroke,including cerebral ischemia,intracerebral hemorrhage,and subarachnoid hemorrhage,is the leading cause of long-term disability and death worldwide. Animal models have greatly contributed to our understanding of the risk factors and the pathophysiology of stroke,as well as the development of therapeutic strategies for its treatment. Further development and investigation of experimental models,however,are needed to elucidate the pathogenesis of stroke and to enhance and expand novel therapeutic targets. In this article,we provide an overview of the characteristics of commonly-used animal models of stroke and focus on the infl ammatory responses to cerebral stroke,which may provide insights into a framework for developing effective therapies for stroke in humans. | Tao Yan Michael Chopp Jieli Chen | 2015 | Neuroscience Bulletin2015，31，6： | 26 |
| 3 | Emerging potential of exosomes for treatment of traumatic brain injury显示文摘Traumatic brain injury(TBI) is one of the major causes of death and disability worldwide.No effective treatment has been identified from clinical trials.Compelling evidence exists that treatment with mesenchymal stem cells(MSCs) exerts a substantial therapeutic effect after experimental brain injury.In addition to their soluble factors,therapeutic effects of MSCs may be attributed to their generation and release of exosomes.Exosomes are endosomal origin small-membrane nano-sized vesicles generated by almost all cell types.Exosomes play a pivotal role in intercellular communication.Intravenous delivery of MSC-derived exosomes improves functional recovery and promotes neuroplasticity in rats after TBI.Therapeutic effects of exosomes derive from the exosome content,especially micro RNAs(mi RNAs).mi RNAs are small non-coding regulatory RNAs and play an important role in posttranscriptional regulation of genes.Compared with their parent cells,exosomes are more stable and can cross the blood-brain barrier.They have reduced the safety risks inherent in administering viable cells such as the risk of occlusion in microvasculature or unregulated growth of transplanted cells.Developing a cell-free exosome-based therapy may open up a novel approach to enhancing multifaceted aspects of neuroplasticity and to amplifying neurological recovery,potentially for a variety of neural injuries and neurodegenerative diseases.This review discusses the most recent knowledge of exosome therapies for TBI,their associated challenges and opportunities. | Ye Xiong Asim Mahmood Michael Chopp | 2017 | Neural Regeneration Research2017，12，1： | 22 |
| 4 | Current understanding of neuroinflammation after traumatic brain injury and cell-based therapeutic opportunities显示文摘 | Ye Xiong Asim Mahmood Michael Chopp | 2018 | Chinese Journal of Traumatology2018，21，3： | 19 |
| 5 | Role of the glymphatic system in ageing and diabetes mellitus impaired cognitive function显示文摘Diabetes mellitus (DM) is a common metabolic disease in the middle-aged and older population, and is associated with cognitive impairment and an increased risk of developing dementia. The glymphatic system is a recently characterised brain-wide cerebrospinal fluid and interstitial fluid drainage pathway that enables the clearance of interstitial metabolic waste from the brain parenchyma. Emerging data suggest that DM and ageing impair the glymphatic system, leading to accumulation of metabolic wastes including amyloid-β within the brain parenchyma, and consequently provoking cognitive dysfunction. In this review, we concisely discuss recent findings regarding the role of the glymphatic system in DM and ageing associated cognitive impairment. | Li Zhang Michael Chopp Quan Jiang Zhenggang Zhang | 2019 | Stroke & Vascular Neurology2019，4，2： | 6 |
| 6 | Axonal remodeling of the corticospinal tract during neurological recovery after stroke显示文摘Stroke remains the leading cause of long-term disability.Hemiparesis is one of the most common post-stroke motor deficits and is largely attributed to loss or disruption of the motor signals from the affected motor cortex.As the only direct descending motor pathway,the corticospinal tract(CST)is the primary pathway to innervate spinal motor neurons,and thus,forms the neuroanatomical basis to control the peripheral muscles for voluntary movements.Here,we review evidence from both experimental animals and stroke patients,regarding CST axonal damage,functional contribution of CST axonal integrity and remodeling to neurological recovery,and therapeutic approaches aimed to enhance CST axonal remodeling after stroke.The new insights gleaned from preclinical and clinical studies may encourage the development of more rational therapeutics with a strategy targeted to promote axonal rewiring for corticospinal innervation,which will significantly impact the current clinical needs of subacute and chronic stroke treatment. | Zhongwu Liu Hongqi Xin Michael Chopp | 2021 | Neural Regeneration Research2021，16，5： | 6 |
| 7 | PDE5 inhibitors promote recovery of peripheral neuropathy in diabetic mice显示文摘Diabetes mellitus affects an estimated 422 million people worldwide.Peripheral neuropathy is one of the most common and disabling complications of diabetes.There is currently no effective treatment for diabetic neuropathy,even with diligent blood | Lei Wang Michael Chopp Zheng Gang Zhang | 2017 | Neural Regeneration Research2017，12，2： | 5 |
| 8 | Remodeling dendritic spines for treatment of traumatic brain injury显示文摘Traumatic brain injury is an important global public health problem.Traumatic brain injury not only causes neural cell death,but also induces dendritic spine degeneration.Spared neurons from cell death in the injured brain may exhibit dendrite damage,dendritic spine degeneration,mature spine loss,synapse loss,and impairment of activity.Dendritic degeneration and synapse loss may significantly contribute to functional impairments and neurological disorders following traumatic brain injury.Normal function of the nervous system depends on maintenance of the functionally intact synaptic connections between the presynaptic and postsynaptic spines from neurons and their target cells.During synaptic plasticity,the numbers and shapes of dendritic spines undergo dynamic reorganization.Enlargement of spine heads and the formation and stabilization of new spines are associated with long-term potentiation,while spine shrinkage and retraction are associated with long-term depression.Consolidation of memory is associated with remodeling and growth of preexisting synapses and the formation of new synapses.To date,there is no effective treatment to prevent dendritic degeneration and synapse loss.This review outlines the current data related to treatments targeting dendritic spines that propose to enhance spine remodeling and improve functional recovery after traumatic brain injury.The mechanisms underlying proposed beneficial effects of therapy targeting dendritic spines remain elusive,possibly including blocking activation of Cofilin induced by beta amyloid,Ras activation,and inhibition of GSK-3 signaling pathway.Further understanding of the molecular and cellular mechanisms underlying synaptic degeneration/loss following traumatic brain injury will advance the understanding of the pathophysiology induced by traumatic brain injury and may lead to the development of novel treatments for traumatic brain injury. | Ye Xiong Asim Mahmood Michael Chopp | 2019 | Neural Regeneration Research2019，14，9： | 4 |
| 9 | Reactive astrocytes promote axonal remodeling and neurological recovery after stroke显示文摘Stroke is a leading cause of death and disability in adults worldwide.For decades,the primary approach and goal of therapy for stroke has focused on neuroprotection,namely treating the injured tissue,with interventions designed to reduce the volume of cerebral infarction.Enormous effort in the laboratory has been devoted to the development | Zhongwu Liu Hongqi Xin Michael Chopp | 2014 | Neural Regeneration Research2014，9，21： | 4 |
| 10 | Exosome‐Mediated Transfer of miR‐133b from Multipotent Mesenchymal Stromal Cells to Neural Cells Contributes to Neurite Outgrowth显示文摘 | Hongqi Xin Yi Li Ben Buller Mark Katakowski Yi Zhang Xinli Wang Xia Shang Zheng Gang Zhang Michael Chopp | 2012 | STEM CELLS2012，，7： | 2 |
| 11 | 神经营养素与中枢神经系统损伤后突触的再生修复显示文摘突触的再生修复是细胞水平上中枢神经系统损伤后再生修复的重要组成部分之一。神经营养素能够通过多种机制调节突触的再生修复,增强突触的功效,促进中枢神经系统损伤的修复。深入了解神经营养素对突触的结构和功能的作用机制,探索最佳用药方法和途径,将有效促进损伤的中枢神经功能的恢复。 | 安沂华 江涛 Dunyue Lu Michael Chopp | 2004 | 中国微侵袭神经外科杂志2004，9，1： | 2 |
| 12 | Therapeutic Benefit of Intravenous Administration of Bone Marrow Stromal Cells After Cerebral Ischemia in Rats显示文摘 | Jieli Chen Yi Li Lei Wang Zhenggang Zhang Dunyue Lu Mei Lu Michael Chopp | 2001 | Stroke: Journal of the American Heart Association2001，，4： | 2 |
| 13 | Microvascular structure after embolic focal cerebral ischemia in the rat显示文摘 | Daniel C. Morris Thomas Yeich Mohammad Mehdi Khalighi Hamid Soltanian-Zadeh Zheng G. Zhang Michael Chopp | 2003 | Brain Research2003，，1： | 1 |
| 14 | Treatment of Traumatic Brain Injury in Adult Rats with Intravenous Administration of Human Bone Marrow Stromal Cells显示文摘 | Asim Mahmood Dunyue Lu Mei Lu Michael Chopp | 2003 | Neurosurgery2003，，3： | 1 |
| 15 | Treatment of neural injury with marrow stromal cells显示文摘 | Michael Chopp Yi Li | 2002 | Lancet Neurology2002，，2： | 1 |
| 16 | The therapeutic effects of cellular therapy for functional recovery after brain injury显示文摘 | Richard L Harvey Michael Chopp | 2003 | Physical Medicine & Rehabilitation Clinics of North America2003，，1： | 1 |
| 17 | Delayed Administration of Human Umbilical Tissue-Derived Cells Improved Neurological Functional Recovery in a Rodent Model of Focal Ischemia显示文摘 | Li Zhang Yi Li Chunling Zhang Michael Chopp Anna Gosiewska Klaudyne Hong | 2011 | Stroke A Journal of Cerebral Circulation2011，，5： | 1 |
| 18 | Marrow stromal cell transplantation in stroke and traumatic brain injury显示文摘 | Yi Li Michael Chopp | 2009 | Neuroscicncc Letters2009，456，3： | 1 |
| 19 | Early Prediction of Gross Hemorrhagic Transformation by Noncontrast Agent MRI Cluster Analysis After Embolic Stroke in Rat显示文摘 | Guangliang Ding Vijaya Nagesh Quan Jiang Li Zhang Zheng Gang Zhang Lian Li Robert A. Knight Qingjiang Li James R. Ewing Michael Chopp | 2005 | Stroke2005，，6： | 1 |
| 20 | Cerebral vessels express interleukin 1 β after focal cerebral ischemia显示文摘 | Zhenggang Zhang Michael Chopp Anton Goussev Cecylia Powers | 1998 | Brain Research1998，，1： | 1 |
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