miR‐223 promotes regenerative myeloid cell phenotype and function in the demyelinated central nervous system

Glia ◽  
2018 ◽  
Vol 67 (5) ◽  
pp. 857-869 ◽  
Author(s):  
Dylan A. Galloway ◽  
Stephanie N. Blandford ◽  
Tangyne Berry ◽  
John B. Williams ◽  
Mark Stefanelli ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Myeloid Cell ◽  
Cell Phenotype ◽  
And Function

scholarly journals The Past, Present and Future of Flow Cytometry in Central Nervous System Malignancies

2021 ◽  
Vol 4 (1) ◽  
pp. 11
Author(s):  
Evrysthenis Vartholomatos ◽  
George Vartholomatos ◽  
George A. Alexiou ◽  
Georgios S. Markopoulos
Keyword(s):  
Central Nervous System ◽  
Flow Cytometry ◽  
Nervous System ◽  
Therapeutic Agents ◽  
Phenotypic Characterization ◽  
Cell Phenotype ◽  
Analytical Technique ◽  
The Past ◽  
Current Review

Central nervous system malignancies (CNSMs) are categorized among the most aggressive and deadly types of cancer. The low median survival in patients with CNSMs is partly explained by the objective difficulties of brain surgeries as well as by the acquired chemoresistance of CNSM cells. Flow Cytometry is an analytical technique with the ability to quantify cell phenotype and to categorize cell populations on the basis of their characteristics. In the current review, we summarize the Flow Cytometry methodologies that have been used to study different phenotypic aspects of CNSMs. These include DNA content analysis for the determination of malignancy status and phenotypic characterization, as well as the methodologies used during the development of novel therapeutic agents. We conclude with the historical and current utility of Flow Cytometry in the field, and we propose how we can exploit current and possible future methodologies in the battle against this dreadful type of malignancy.

Subcellular localization and function of mouse radial spoke protein 3 in mammalian cells and central nervous system

2014 ◽  
Vol 45 (6) ◽  
pp. 723-732 ◽  
Author(s):  
Xinde Hu ◽  
Runchuan Yan ◽  
Lingzhen Song ◽  
Xi Lu ◽  
Shulin Chen ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Subcellular Localization ◽  
Mammalian Cells ◽  
Radial Spoke ◽  
And Function

scholarly journals Amino acid sequence of the encephalitogenic basic protein from human myelin

1971 ◽  
Vol 123 (1) ◽  
pp. 57-67 ◽  
Author(s):  
P. R. Carnegie
Keyword(s):  
Amino Acids ◽  
Central Nervous System ◽  
Nervous System ◽  
Amino Acid ◽  
Basic Protein ◽  
Structure And Function ◽  
Autoimmune Encephalomyelitis ◽  
The Central Nervous System ◽  
And Function ◽  
Experimental Autoimmune

Myelin from the central nervous system contains an unusual basic protein, which can induce experimental autoimmune encephalomyelitis. The basic protein from human brain was digested with trypsin and other enzymes and the sequence of the 170 amino acids was determined. The localization of the encephalitogenic determinants was described. Possible roles for the protein in the structure and function of myelin are discussed.

scholarly journals Interferon β-Mediated Protective Functions of Microglia in Central Nervous System Autoimmunity

2019 ◽  
Vol 20 (1) ◽  
pp. 190 ◽  
Author(s):  
Stefanie Scheu ◽  
Shafaqat Ali ◽  
Ritu Mann-Nüttel ◽  
Lisa Richter ◽  
Volker Arolt ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Molecular Mechanisms ◽  
Chronic Inflammatory Disease ◽  
Clinical Severity ◽  
Interferon Β ◽  
Treatment Regimens ◽  
Cns Autoimmunity ◽  
And Function ◽  
The Impact

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS) leading to demyelination and axonal damage. It often affects young adults and can lead to neurological disability. Interferon β (IFNβ) preparations represent widely used treatment regimens for patients with relapsing-remitting MS (RRMS) with therapeutic efficacy in reducing disease progression and frequency of acute exacerbations. In mice, IFNβ therapy has been shown to ameliorate experimental autoimmune encephalomyelitis (EAE), an animal model of MS while genetic deletion of IFNβ or its receptor augments clinical severity of disease. However, the complex mechanism of action of IFNβ in CNS autoimmunity has not been fully elucidated. Here, we review our current understanding of the origin, phenotype, and function of microglia and CNS immigrating macrophages in the pathogenesis of MS and EAE. In addition, we highlight the emerging roles of microglia as IFNβ-producing cells and vice versa the impact of IFNβ on microglia in CNS autoimmunity. We finally discuss recent progress in unraveling the underlying molecular mechanisms of IFNβ-mediated effects in EAE.

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