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Article ; Online: Oligodendrocyte Lineage Marker Expression in eGFP-GFAP Transgenic Mice.

Behrangi, Newshan / Lorenz, Peter / Kipp, Markus

2020 Volume 71, Issue 11, Page(s) 2237–2248

Abstract: Oligodendrocytes, the myelinating cells of the central nervous system, orchestrate several key cellular functions in the brain and spinal cord, including axon insulation, energy transfer to neurons, and, eventually, modulation of immune responses. There ... ...

Abstract	Oligodendrocytes, the myelinating cells of the central nervous system, orchestrate several key cellular functions in the brain and spinal cord, including axon insulation, energy transfer to neurons, and, eventually, modulation of immune responses. There is growing interest for obtaining reliable markers that can specifically label oligodendroglia and their progeny. In many studies, anti-CC1 antibodies, presumably recognizing the protein adenomatous polyposis coli (APC), are used to label mature, myelinating oligodendrocytes. However, it has been discussed whether anti-CC1 antibodies could recognize as well, under pathological conditions, other cell populations, particularly astrocytes. In this study, we used transgenic mice in which astrocytes are labeled by the enhanced green fluorescent protein (eGFP) under the control of the human glial fibrillary acidic protein (GFAP) promoter. By detailed co-localization studies we were able to demonstrate that a significant proportion of eGFP-expressing cells co-express markers of the oligodendrocyte lineage, such as the transcription factor Oligodendrocyte Transcription Factor 2 (OLIG2); the NG2 proteoglycan, also known as chrondroitin sulfate proteoglycan 4 (CSPG4); or APC. The current finding that the GFAP promoter drives transgene expression in cells of the oligodendrocyte lineage should be considered when interpreting results from co-localization studies.
MeSH term(s)	Animals ; Cell Lineage ; Genes, Reporter ; Glial Fibrillary Acidic Protein/genetics ; Glial Fibrillary Acidic Protein/metabolism ; Green Fluorescent Proteins/genetics ; Green Fluorescent Proteins/metabolism ; Mice ; Mice, Inbred C57BL ; Oligodendroglia/cytology ; Oligodendroglia/metabolism ; Promoter Regions, Genetic ; Recombinant Proteins/genetics ; Recombinant Proteins/metabolism ; Transgenes
Chemical Substances	Glial Fibrillary Acidic Protein ; Recombinant Proteins ; glial fibrillary astrocytic protein, mouse ; Green Fluorescent Proteins (147336-22-9)
Language	English
Publishing date	2020-12-21
Publishing country	United States
Document type	Journal Article
ZDB-ID	1043392-2
ISSN	1559-1166 ; 0895-8696
ISSN (online)	1559-1166
ISSN	0895-8696
DOI	10.1007/s12031-020-01771-w
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Zs.A 3006: Show issues

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Book ; Online ; Thesis: Phenotypes and glia-immune cell interactions in animal models of multiple sclerosis

Behrangi, Newshan [Verfasser] / Kipp, Markus [Akademischer Betreuer]

2021

Author's details	Newshan Behrangi ; Betreuer: Markus Kipp
Keywords	Medizin, Gesundheit ; Medicine, Health
Subject code	sg610
Language	English
Publisher	Universitätsbibliothek der Ludwig-Maximilians-Universität
Publishing place	München
Document type	Book ; Online ; Thesis
Database	Digital theses on the web

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Article: Mechanism of Siponimod: Anti-Inflammatory and Neuroprotective Mode of Action.

Behrangi, Newshan / Fischbach, Felix / Kipp, Markus

Cells

2019 Volume 8, Issue 1

Abstract: Multiple sclerosis (MS) is a neuroinflammatory disorder of the central nervous system (CNS), and represents one of the main causes of disability in young adults. On the histopathological level, the disease is characterized by inflammatory demyelination ... ...

Abstract	Multiple sclerosis (MS) is a neuroinflammatory disorder of the central nervous system (CNS), and represents one of the main causes of disability in young adults. On the histopathological level, the disease is characterized by inflammatory demyelination and diffuse neurodegeneration. Although on the surface the development of new inflammatory CNS lesions in MS may appear consistent with a primary recruitment of peripheral immune cells, questions have been raised as to whether lymphocyte and/or monocyte invasion into the brain are really at the root of inflammatory lesion development. In this review article, we discuss a less appreciated inflammation-neurodegeneration interplay, that is: Neurodegeneration can trigger the formation of new, focal inflammatory lesions. We summarize old and recent findings suggesting that new inflammatory lesions develop at sites of focal or diffuse degenerative processes within the CNS. Such a concept is discussed in the context of the EXPAND trial, showing that siponimod exerts anti-inflammatory and neuroprotective activities in secondary progressive MS patients. The verification or rejection of such a concept is vital for the development of new therapeutic strategies for progressive MS.
MeSH term(s)	Adolescent ; Adult ; Anti-Inflammatory Agents/pharmacology ; Anti-Inflammatory Agents/therapeutic use ; Azetidines/pharmacology ; Azetidines/therapeutic use ; Benzyl Compounds/pharmacology ; Benzyl Compounds/therapeutic use ; Central Nervous System/drug effects ; Central Nervous System/pathology ; Disease Progression ; Humans ; Middle Aged ; Multiple Sclerosis, Chronic Progressive/drug therapy ; Neuroprotection/drug effects ; Neuroprotective Agents/pharmacology ; Neuroprotective Agents/therapeutic use ; Young Adult
Chemical Substances	Anti-Inflammatory Agents ; Azetidines ; Benzyl Compounds ; Neuroprotective Agents ; siponimod (RR6P8L282I)
Language	English
Publishing date	2019-01-07
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2661518-6
ISSN	2073-4409
ISSN	2073-4409
DOI	10.3390/cells8010024
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Article ; Online: The Cuprizone Model: Dos and Do Nots.

Zhan, Jiangshan / Mann, Teresa / Joost, Sarah / Behrangi, Newshan / Frank, Marcus / Kipp, Markus

Cells

2020 Volume 9, Issue 4

Abstract: Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system. Various pre-clinical models with different specific features of the disease are available to study MS pathogenesis and to develop new therapeutic ... ...

Abstract	Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system. Various pre-clinical models with different specific features of the disease are available to study MS pathogenesis and to develop new therapeutic options. During the last decade, the model of toxic demyelination induced by cuprizone has become more and more popular, and it has contributed substantially to our understanding of distinct yet important aspects of the MS pathology. Here, we aim to provide a practical guide on how to use the cuprizone model and which pitfalls should be avoided.
MeSH term(s)	Animals ; Body Weight/drug effects ; Cuprizone/toxicity ; Demyelinating Diseases/genetics ; Demyelinating Diseases/pathology ; Disease Models, Animal ; Gene Expression Regulation ; Multiple Sclerosis/chemically induced ; Multiple Sclerosis/genetics ; Multiple Sclerosis/pathology
Chemical Substances	Cuprizone (5N16U7E0AO)
Language	English
Publishing date	2020-03-31
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells9040843
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Article ; Online: [

Müller, Luisa / Power Guerra, Nicole / Schildt, Anna / Lindner, Tobias / Stenzel, Jan / Behrangi, Newshan / Bergner, Carina / Alberts, Teresa / Bühler, Daniel / Kurth, Jens / Krause, Bernd Joachim / Janowitz, Deborah / Teipel, Stefan / Vollmar, Brigitte / Kuhla, Angela

Biomolecules

2023 Volume 13, Issue 5

Abstract: Obesity is characterized by immoderate fat accumulation leading to an elevated risk of neurodegenerative disorders, along with a host of metabolic disturbances. Chronic neuroinflammation is a main factor linking obesity and the propensity for ... ...

Abstract	Obesity is characterized by immoderate fat accumulation leading to an elevated risk of neurodegenerative disorders, along with a host of metabolic disturbances. Chronic neuroinflammation is a main factor linking obesity and the propensity for neurodegenerative disorders. To determine the cerebrometabolic effects of diet-induced obesity (DIO) in female mice fed a long-term (24 weeks) high-fat diet (HFD, 60% fat) compared to a group on a control diet (CD, 20% fat), we used in vivo PET imaging with the radiotracer [
MeSH term(s)	Mice ; Female ; Animals ; Diet, High-Fat/adverse effects ; Neuroinflammatory Diseases ; Obesity/diagnostic imaging ; Obesity/metabolism ; Carrier Proteins ; Neurodegenerative Diseases ; Glucose ; Positron-Emission Tomography/methods ; Mice, Inbred C57BL
Chemical Substances	GE-180 ; Carrier Proteins ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2023-04-28
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2701262-1
ISSN	2218-273X ; 2218-273X
ISSN (online)	2218-273X
ISSN	2218-273X
DOI	10.3390/biom13050769
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Article ; Online: Siponimod ameliorates metabolic oligodendrocyte injury via the sphingosine-1 phosphate receptor 5.

Behrangi, Newshan / Heinig, Leo / Frintrop, Linda / Santrau, Emily / Kurth, Jens / Krause, Bernd / Atanasova, Dimitrinka / Clarner, Tim / Fragoulis, Athanassios / Joksch, Markus / Rudolf, Henrik / Meuth, Sven G / Joost, Sarah / Kipp, Markus

Proceedings of the National Academy of Sciences of the United States of America

2022 Volume 119, Issue 40, Page(s) e2204509119

Abstract: Multiple sclerosis (MS), an autoimmune-driven, inflammatory demyelinating disease of the central nervous system (CNS), causes irreversible accumulation of neurological deficits to a variable extent. Although there are potent disease-modifying agents for ... ...

Abstract	Multiple sclerosis (MS), an autoimmune-driven, inflammatory demyelinating disease of the central nervous system (CNS), causes irreversible accumulation of neurological deficits to a variable extent. Although there are potent disease-modifying agents for its initial relapsing-remitting phase, immunosuppressive therapies show limited efficacy in secondary progressive MS (SPMS). Although modulation of sphingosine-1 phosphate receptors has proven beneficial during SPMS, the underlying mechanisms are poorly understood. In this project, we followed the hypothesis that siponimod, a sphingosine-1 phosphate receptor modulator, exerts protective effects by direct modulation of glia cell function (i.e., either astrocytes, microglia, or oligodendrocytes). To this end, we used the toxin-mediated, nonautoimmune MS animal model of cuprizone (Cup) intoxication. On the histological level, siponimod ameliorated cuprizone-induced oligodendrocyte degeneration, demyelination, and axonal injury. Protective effects were evident as well using GE180 translocator protein 18-kDa (TSPO) imaging with positron emission tomography (PET)/computed tomography (CT) imaging or next generation sequencing (NGS). Siponimod also ameliorated the cuprizone-induced pathologies in
MeSH term(s)	Animals ; Azetidines/pharmacology ; Benzyl Compounds/pharmacology ; Cuprizone ; Disease Models, Animal ; Homeodomain Proteins/genetics ; Mice ; Mice, Inbred C57BL ; Multiple Sclerosis, Chronic Progressive/drug therapy ; Oligodendroglia/drug effects ; Sphingosine/pharmacology ; Sphingosine/therapeutic use ; Sphingosine-1-Phosphate Receptors/metabolism
Chemical Substances	Azetidines ; Benzyl Compounds ; Homeodomain Proteins ; Sphingosine-1-Phosphate Receptors ; RAG-1 protein (128559-51-3) ; Cuprizone (5N16U7E0AO) ; Sphingosine (NGZ37HRE42) ; siponimod (RR6P8L282I)
Language	English
Publishing date	2022-09-26
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2204509119
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Zs.A 1148: Show issues

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Article ; Online: Laquinimod ameliorates secondary brain inflammation.

Nedelcu, Julia / Reinbach, Christin / Riedler, Philipp / Brendel, Matthias / Rominger, Axel / Kaye, Joel / Behrangi, Newshan / Jiangshan, Zhan / Schmitz, Christoph / Kipp, Markus

Neurobiology of disease

2019 Volume 134, Page(s) 104675

Abstract: Accumulating evidence suggests that a degenerative processes within the brain can trigger the formation of new, focal inflammatory lesions in Multiple Sclerosis (MS). Here, we used a novel pre-clinical MS animal model to test whether the amelioration of ... ...

Abstract	Accumulating evidence suggests that a degenerative processes within the brain can trigger the formation of new, focal inflammatory lesions in Multiple Sclerosis (MS). Here, we used a novel pre-clinical MS animal model to test whether the amelioration of degenerative brain events reduces the secondary recruitment of peripheral immune cells and, in consequence, inflammatory lesion development. Neural degeneration was induced by a 3 weeks cuprizone intoxication period. To mitigate the cuprizone-induced pathology, animals were treated with Laquinimod (25 mg/kg) during the cuprizone-intoxication period. At the beginning of week 6, encephalitogenic T cell development in peripheral lymphoid organs was induced by the immunization with myelin oligodendrocyte glycoprotein 35-55 peptide (i.e., Cup/EAE). Demyelination, axonal injury and reactive gliosis were determined by immunohistochemistry. Positron emission tomography (PET) imaging was performed to analyze glia activation in vivo. Vehicle-treated cuprizone mice displayed extensive callosal demyelination, glia activation and enhanced TSPO-ligand binding. This cuprizone-induced pathology was profoundly ameliorated in mice treated with Laquinimod. In vehicle-treated Cup/EAE mice, the cuprizone-induced pathology triggered massive peripheral immune cell recruitment into the forebrain, evidenced by multifocal perivascular inflammation, glia activation and neuro-axonal injury. While anti myelin oligodendrocyte glycoprotein 35-55 peptide immune responses were comparable in vehicle- and Laquinimod-treated Cup/EAE mice, the cuprizone-triggered immune cell recruitment was ameliorated by the Laquinimod treatment. This study clearly illustrates that amelioration of a primary brain-intrinsic degenerative process secondary halts peripheral immune cell recruitment and, in consequence, inflammatory lesion development. These findings have important consequences for the interpretation of the results of clinical studies.
MeSH term(s)	Animals ; Brain/drug effects ; Brain/pathology ; Cuprizone/administration & dosage ; Disease Models, Animal ; Encephalitis/chemically induced ; Encephalitis/immunology ; Encephalitis/pathology ; Female ; Gliosis/chemically induced ; Gliosis/pathology ; Mice, Inbred C57BL ; Multiple Sclerosis/immunology ; Multiple Sclerosis/pathology ; Quinolones/administration & dosage
Chemical Substances	Quinolones ; Cuprizone (5N16U7E0AO) ; laquinimod (908SY76S4G)
Language	English
Publishing date	2019-11-13
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1211786-9
ISSN	1095-953X ; 0969-9961
ISSN (online)	1095-953X
ISSN	0969-9961
DOI	10.1016/j.nbd.2019.104675
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Article ; Online: Continuous cuprizone intoxication allows active experimental autoimmune encephalomyelitis induction in C57BL/6 mice.

Yakimov, Vladislav / Schweiger, Felix / Zhan, Jiangshan / Behrangi, Newshan / Horn, Anja / Schmitz, Christoph / Hochstrasser, Tanja / Kipp, Markus

Histochemistry and cell biology

2019 Volume 152, Issue 2, Page(s) 119–131

Abstract: Oligodendrocyte degeneration is a hallmark of multiple sclerosis pathology, and protecting oligodendrocytes and myelin is likely to be of clinical relevance. Traditionally, oligodendrocyte and myelin degeneration are viewed as a direct consequence of an ... ...

Abstract	Oligodendrocyte degeneration is a hallmark of multiple sclerosis pathology, and protecting oligodendrocytes and myelin is likely to be of clinical relevance. Traditionally, oligodendrocyte and myelin degeneration are viewed as a direct consequence of an inflammatory attack, but metabolic defects might be equally important. Appropriate animal models to study the interplay of inflammation and metabolic injury are, therefore, needed. Here, we describe that in spite of its immunosuppressive effects, a continuous intoxication with cuprizone allows the induction of active experimental autoimmune encephalomyelitis (EAE) by myelin oligodendrocyte glycoprotein (MOG
MeSH term(s)	Administration, Oral ; Animals ; Apoptosis/drug effects ; Apoptosis/immunology ; Cuprizone/administration & dosage ; Cuprizone/toxicity ; Encephalomyelitis, Autoimmune, Experimental/chemically induced ; Encephalomyelitis, Autoimmune, Experimental/immunology ; Encephalomyelitis, Autoimmune, Experimental/pathology ; Female ; Mice ; Mice, Inbred C57BL ; Myelin-Oligodendrocyte Glycoprotein/immunology ; Oligodendroglia/drug effects ; Oligodendroglia/immunology ; Oligodendroglia/pathology ; Peptide Fragments/immunology
Chemical Substances	Myelin-Oligodendrocyte Glycoprotein ; Peptide Fragments ; myelin oligodendrocyte glycoprotein (35-55) ; Cuprizone (5N16U7E0AO)
Language	English
Publishing date	2019-04-23
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1222930-1
ISSN	1432-119X ; 0301-5564 ; 0948-6143
ISSN (online)	1432-119X
ISSN	0301-5564 ; 0948-6143
DOI	10.1007/s00418-019-01786-4
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Article ; Online: MMP9 Gene Expression Variation by Ingesting Tart Cherry and P-Coumaric Acid During Remyelination in the Cuprizone Mouse Model.

Behrangi, Newshan / Namvar, Nabiyollah / Ataei, Mitra / Dizaji, Sakineh / Javdani, Golshid / Sanati, Mahommad Hossein

Acta medica Iranica

2017 Volume 55, Issue 9, Page(s) 539–549

Abstract: Matrix metalloproteinase-9 (GELB) as a member of gelatinases plays key role in the destruction of blood-brain barrier (BBB), T cells migration into the CNS, and demyelination induction. Considering remyelination induction in response to tart cherry ... ...

Abstract	Matrix metalloproteinase-9 (GELB) as a member of gelatinases plays key role in the destruction of blood-brain barrier (BBB), T cells migration into the CNS, and demyelination induction. Considering remyelination induction in response to tart cherry extract and pure p-coumaric acid ingestion via tracking MMP9 gene expression in the cuprizone mouse model. Firstly, predicting the chemical interaction between p-coumaric acid and MMP9 protein was conducted through PASS and Swiss dock web services. Next, the content of p-coumaric acid in the tart cherry extract was analyzed by HPLC. Later, mice (male, female) were categorized into two groups: standard, cuprizone. After the demyelination period, mice classified into four groups: standard, natural chow, tart cherry extract, p-coumaric acid. Finally, brains were extracted from the skull, and MMP9 gene expression was evaluated by real time RT-PCR. Bioinformatics analysis displayed p-coumaric acid has potent inhibitory effect on MMP9 gene expression (Pa=0.818) with estimated ΔG (kcal/mol) -8.10. In addition, during the demyelination period, MMP9 expression was increased significantly in the male group that is related to myelin destruction. However, MMP9 was declined throughout remyelination in both male and female. It's remarkable that pure p-coumaric acid and tart cherry extract ingestion could decrease the gene expression ratio more than natural chow. According to the results, it's deduced the male mouse is more appropriate gender for demyelination induction via cuprizone. In addition, tart cherry extract and pure p-coumaric acid ingestion could decrease MMP9 gene expression level considerably during remyelination.
MeSH term(s)	Animals ; Brain/metabolism ; Cuprizone/administration & dosage ; Demyelinating Diseases ; Disease Models, Animal ; Female ; Male ; Matrix Metalloproteinase 9/genetics ; Mice ; Mice, Inbred C57BL ; Myelin Sheath/metabolism ; Propionates/pharmacology ; Remyelination
Chemical Substances	Propionates ; Cuprizone (5N16U7E0AO) ; Matrix Metalloproteinase 9 (EC 3.4.24.35) ; Mmp9 protein, mouse (EC 3.4.24.35) ; p-coumaric acid (IBS9D1EU3J)
Language	English
Publishing date	2017-12-01
Publishing country	Iran
Document type	Journal Article
ZDB-ID	603042-7
ISSN	1735-9694 ; 0044-6025
ISSN (online)	1735-9694
ISSN	0044-6025
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