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Emerging roles of astrocytes in blood-brain barrier disruption upon amyloid-beta insults in Alzheimer's disease

Neural Regeneration Research 2023年第9期18卷 1890-1902页

作者： Qian Yue Maggie Pui Man Hoi State Key Laboratory of Quality Research in Chinese Medicine Institute of Chinese Medical SciencesUniversity of MacaoMacao Special Administrative RegionChina Department of Pharmaceutical Sciences Faculty of Health SciencesUniversity of MacaoMacao Special Administrative RegionChina

Blood-brain barrier disruption occurs in the early stages of Alzheimer’s disease.Recent studies indicate a link between blood-brain barrier dysfunction and cognitive decline and might accelerate Alzheimer’s disease progression.astrocytes are the most abundant glial cells in the central nervous system with important roles in the structural and functional maintenance of the blood-brain barrier.For example,astrocytic cove rage around endothelial cells with perivascular endfeet and secretion of homeostatic soluble factors are two major underlying mechanisms of astrocytic physiological functions.astrocyte activation is often observed in Alzheimer’s disease patients,with astrocytes expressing a high level of glial fibrillary acid protein detected around amyloid-beta plaque with the elevated phagocytic ability for amyloid-beta.Structural alte rations in Alzheimer’s disease astrocytes including swollen endfeet,somata shrinkage and possess loss contribute to disruption in vascular integrity at capillary and arte rioles levels.In addition,Alzheimer’s disease astrocytes are skewed into proinflammatory and oxidative profiles with increased secretions of vasoactive mediators inducing endothelial junction disruption and immune cell infiltration.In this review,we summarize the findings of existing literature on the relevance of astrocyte alte ration in response to amyloid pathology in the context of blood-brain barrier dysfunction.First,we briefly describe the physiological roles of astrocytes in blood-brain barrier maintenance.Then,we review the clinical evidence of astrocyte pathology in Alzheimer’s disease patients and the preclinical evidence in animal and cellular models.We further discuss the structural changes of blood-brain barrier that correlates with Alzheimer’s disease astrocyte.Finally,we evaluate the roles of soluble factors secreted by Alzheimer’s disease astrocytes,providing potential molecular mechanisms underlying blood-brain barrier modulation.We conclude with a perspective on investigating the therapeutic pot

关键词： Alzheimer’s disease amyloid-beta astrocyte(astroglial)-endothelial interaction astrocyte pathology blood-brain barrier blood-brain barrier disruption brain endothelial cell neuroinflammation reactive astrocyte

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A neuron-immune circuit regulates neurodegeneration in the hindbrain and spinal cord of Arf1-ablated mice

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National Science Review 2023年第12期10卷 98-110页

作者： Guohao Wang Shuhan Jin Jiaqi Liu Xu Li Peng Dai Yuetong Wang Steven X.Hou The Basic Research Laboratory Center for Cancer ResearchNational Cancer Institute at FrederickNational Institutes of Health Department of Cell and Developmental Biology at the School of Life Sciences State Key Laboratory of Genetic EngineeringInstitute of Metabolism and Integrative BiologyHuman Phenome Institute Department of Liver Surgery and Transplantation of Liver Cancer Institute at Zhongshan Hospital Fudan University

Neuroimmune connections have been revealed to play a central role in neurodegenerative diseases(NDs).However, the mechanisms that link the central nervous system(CNS) and peripheral immune cells are still mostly unknown. We recently found that specific ablation of the Arf1 gene in hindbrain and spinal cord neurons promoted NDs through activating the NLRP3 inflammasome in microglia via peroxided lipids and adenosine triphosphate(ATP) releasing. Here, we demonstrate that IL-1β with elevated chemokines in the neuronal Arf1-ablated mouse hindbrain and spinal cord recruited and activated γ δ T cells in meninges. The activated γ δ T cells then secreted IFN-γ that entered into parenchyma to activate the microglia-A1astrocyte-C3-neuronal C3a R neurotoxic pathway. Remarkably, the neurodegenerative phenotypes of the neuronal Arf1-ablated mice were strongly ameliorated by IFN-γ or C3 knockout. Finally, we show that the Arf1-reduction-induced neuroimmune-IFN-γ-gliosis pathway exists in human NDs, particularly in amyotrophic lateral sclerosis and multiple sclerosis. Together, our results uncover a previously unknown mechanism that links the CNS and peripheral immune cells to promote neurodegeneration.

关键词： neurodegenerative diseases disease-associated microglia γδT cells reactive astrocyte IFN- γ C3

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Endoplasmic reticulum stress transducer old astrocyte specifically induced substance contributes to astrogliosis after spinal cord injury

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Neural Regeneration Research 2018年第3期13卷 536-540页

作者： Atsushi Takazawa Naosuke Kamei Nobuo Adachi Mitsuo Ochi Department of Orthopaedic Surgery Graduate School of Biomedical & Health Sciences Hiroshima University Medical Center for Translational & Clinical Research Hiroshima University Hospital

Old astrocyte specifically induced substance （OASIS） is an endoplasmic reticulum （ER） stress transducer specifically expressed in astrocytes and osteoblasts. OASIS regulates the differentiation of neural precursor cells into astrocytes in the central nervous system. This study aimed to elucidate the involvement of ER stress responses stimulated via OASIS in astrogliosis following spinal cord injury. In a mouse model of spinal cord contusion injury, OASIS mRNA and protein expression were evaluated at days 7 and 14. A significant increase in OASIS mRNA on day 7 and an increase in protein on days 7 and 14 was observed in injured spinal cords. Immunostaining on day 7 revealed co-localization of OASIS and astrocytes in the periphery of the injury site. Furthermore, anti-OASIS small interfering RNA （siRNA） was injected at the injury sites on day 5 to elucidate the function of OASIS. Treatment with anti-OASIS siRNA caused a significant decrease in OASIS mRNA on day 7 and protein on days 7 and 14, and was associated with the inhibition of astrogliosis and hindlimb motor function recovery. Results of our study show that OASIS expression synchronizes with astrogliosis and is functionally associated with astrogliosis after spinal cord injury.

关键词： unfolded protein response cAMP-response element binding protein/activating transcription factor protein family C57BL/6 contusion injury reactive astrocyte functional recovery real-time polymerase chain reaction western blot immunohistochemistry glial fibrillary acidic protein

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Proliferation and differentiation of reactive nestin^+/GFAP^+ cells in an adult rat model of compression-induced spinal cord injury

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Neural Regeneration Research 2009年第10期4卷 725-731页

作者： Pinglin Yang Xijing He Haopeng Li Binshang Lan Guoyu Wang Yiheng Liu Second Department of Orthopedics Second Affiliated Hospital of Xi'an Jiaotong University Medical School Xi'an 710004 Shaanxi Province China

BACKGROUND： Studies have demonstrated that astrocytes may possess similar properties to neural stem cells/neural precursor cells and have the potential to differentiate into neurons. OBJECTIVE： To observe neuroepithelial stem cell protein （nestin） and glial fibrillary acidic protein （GFAP） expression following spinal cord injury, and to explore whether nestin＋/GFAP＋ cells, which are detected at peak levels in gray and white matter around the ependymal region of the central canal in injured spinal cord, possess similar properties of neural stem cells. DESIGN, TIME AND SETTING： A randomized, controlled experiment. The study was performed at the Key Laboratory of Environment and Genes Related to Diseases （Xi＇an Jiaotong University）, Ministry of Education between January 2004 and December 2006. MATERIALS： Rabbit anti-rat nestin, β-tubulinⅢ, mouse anti-rat GFAP, galactocerebroside （GaLC） antibodies were utilized, as well as flow cytometry. METHODS： A total of 60 male, Sprague Dawley rats, aged 8 weeks, were randomly assigned to control （n = 12） and model （n = 48） groups. The spinal cord injury model was established in the model group by aneurysm clip compression, while the control animals were not treated. The gray and white matter around the ependymal region of the central canal exhibited peak expression of nestin＋/GFAP＋ cells. These cells were harvested and prepared into single cell suspension, followed by primary and passage cultures. The cells were incubated with serum-containing neural stem cell complete medium. MAINOUTCOME MEASURES： Nestin and GFAP expression in injured spinal cord was determined using immunohistochemistry and double-labeled immunofluorescence at 1, 3, 5, 7, 14, 28, and 56 days post-injury. In addition, cell proliferation and differentiation were detected using immunofluorescence cytochemistry and flow cytometry. RESULTS： Compared with the control group, the model group exhibited significantly increased nestin and GFAP expression （P 〈 0.05）, which reached peak levels between 3 and 7 days. The m

关键词： reactive astrocyte neural stem cell spinal cord injury nestin glial fibrillary acidic protein

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Seek consensus on criteria defining a successful reprogrammed cell as neuron

Seek consensus on criteria defining a successful reprogramme...

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中国神经科学学会第十二届全国学术会议

作者： Gangyi Wu School of Life Science South China Normal University

Regenerating functional neurons, via either induced-pluripotent stem cells（i PSCs） or direct somatic reprogramming has enormous potential for cell-based therapies against acute brain injuries or chronic neurodegenerative diseases. Despite recent rapid progress in this exciting field, currently various published methods or protocols vary greatly in their efficacy, purity and maturation status of the reprogrammed neurons, posing a significant hurdle for the field to move forward. Here, I will first discuss the pressing need to establish the criteria defining a successful reprogrammed cell as neuron. I then will demonstrate the utility of an AAV-based conversion of reactive astrocytes into functional GABAergic neurons to rescue the pathological and functional deficits in a mouse model of epilepsy.

关键词： Cell reprogramming brain repair reactive astrocyte GABAergic neuron mouse model of epilepsy

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