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Article: Current Insights Into Oligodendrocyte Metabolism and Its Power to Sculpt the Myelin Landscape.

Narine, Mohanlall / Colognato, Holly

2022 Volume 16, Page(s) 892968

Abstract: Once believed to be part of ... ...

Abstract	Once believed to be part of the
Language	English
Publishing date	2022-04-28
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2452963-1
ISSN	1662-5102
ISSN	1662-5102
DOI	10.3389/fncel.2022.892968
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Article: Brain Dysfunction in LAMA2-Related Congenital Muscular Dystrophy: Lessons From Human Case Reports and Mouse Models.

Arreguin, Andrea J / Colognato, Holly

Frontiers in molecular neuroscience

2020 Volume 13, Page(s) 118

Abstract: Laminin α2 gene (LAMA2)-related Congenital Muscular Dystrophy (CMD) was distinguished by a defining central nervous system (CNS) abnormality-aberrant white matter signals by MRI-when first described in the 1990s. In the past 25 years, researchers and ... ...

Abstract	Laminin α2 gene (LAMA2)-related Congenital Muscular Dystrophy (CMD) was distinguished by a defining central nervous system (CNS) abnormality-aberrant white matter signals by MRI-when first described in the 1990s. In the past 25 years, researchers and clinicians have expanded our knowledge of brain involvement in LAMA2-related CMD, also known as Congenital Muscular Dystrophy Type 1A (MDC1A). Neurological changes in MDC1A can be structural, including lissencephaly and agyria, as well as functional, including epilepsy and intellectual disability. Mouse models of MDC1A include both spontaneous and targeted LAMA2 mutations and range from a partial loss of LAMA2 function (e.g.,
Language	English
Publishing date	2020-07-23
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2452967-9
ISSN	1662-5099
ISSN	1662-5099
DOI	10.3389/fnmol.2020.00118
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Article ; Online: Introduction to the Special Issue on The oligodendrocyte niche in development and repair.

Colognato, Holly / Nishiyama, Akiko

Neuroscience letters

2020 Volume 730, Page(s) 134957

MeSH term(s)	Animals ; Cell Differentiation/physiology ; Cell Lineage/physiology ; Humans ; Oligodendrocyte Precursor Cells/cytology ; Oligodendroglia/cytology ; Research
Language	English
Publishing date	2020-05-01
Publishing country	Ireland
Document type	Editorial ; Introductory Journal Article
ZDB-ID	194929-9
ISSN	1872-7972 ; 0304-3940
ISSN (online)	1872-7972
ISSN	0304-3940
DOI	10.1016/j.neulet.2020.134957
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Article: Investigating demyelination, efficient remyelination and remyelination failure in organotypic cerebellar slice cultures: Workflow and practical tips.

Gorter, Rianne P / Dijksman, Naomi S / Baron, Wia / Colognato, Holly

Methods in cell biology

2022 Volume 168, Page(s) 103–123

Abstract: Healthy myelin is essential for proper brain function. When the myelin sheath is damaged, fast saltatory impulse conduction is lost and neuronal axons become vulnerable to degeneration. Thus, regeneration of the myelin sheath by encouraging ... ...

Abstract	Healthy myelin is essential for proper brain function. When the myelin sheath is damaged, fast saltatory impulse conduction is lost and neuronal axons become vulnerable to degeneration. Thus, regeneration of the myelin sheath by encouraging oligodendrocyte lineage cells to remyelinate the denuded axons is a promising therapeutic target for demyelinating diseases such as multiple sclerosis. Ex vivo organotypic cerebellar slice cultures are a useful model to study developmental myelination, demyelination, remyelination and remyelination failure. In these cultures, the cerebellum's three-dimensional architecture and various cell populations remain largely intact, providing a realistic and relatively cost-efficient model that can be easily manipulated by the addition of viral vectors, pharmaceuticals or (transgenic) cells to augment or replace resident cell populations. Moreover, slice cultures can be treated with lysolecithin or polyinosinic:polycytidylic acid to induce demyelination and mimic efficient as well as inefficient remyelination. It can be challenging to set up slice cultures for the first time, as in our experience, seemingly minor differences in technique and materials can make a great difference to the quality of the cultures. Therefore, this report provides an in-depth description for the generation and maintenance of ex vivo organotypic cerebellar cultures for demyelination-remyelination studies with a focus on practical tips for scientists that are new to this technique.
MeSH term(s)	Cerebellum ; Demyelinating Diseases/drug therapy ; Humans ; Myelin Sheath ; Remyelination/physiology ; Workflow
Language	English
Publishing date	2022-03-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	0091-679X
ISSN	0091-679X
DOI	10.1016/bs.mcb.2021.12.011
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Article: The AMPK activator metformin improves recovery from demyelination by shifting oligodendrocyte bioenergetics and accelerating OPC differentiation.

Narine, Mohanlall / Azmi, Maryam A / Umali, Martin / Volz, Ashley / Colognato, Holly

Frontiers in cellular neuroscience

2023 Volume 17, Page(s) 1254303

Abstract: Multiple Sclerosis (MS) is a chronic disease characterized by immune-mediated destruction of myelinating oligodendroglia in the central nervous system. Loss of myelin leads to neurological dysfunction and, if myelin repair fails, neurodegeneration of the ...

Abstract	Multiple Sclerosis (MS) is a chronic disease characterized by immune-mediated destruction of myelinating oligodendroglia in the central nervous system. Loss of myelin leads to neurological dysfunction and, if myelin repair fails, neurodegeneration of the denuded axons. Virtually all treatments for MS act by suppressing immune function, but do not alter myelin repair outcomes or long-term disability. Excitingly, the diabetes drug metformin, a potent activator of the cellular "energy sensor" AMPK complex, has recently been reported to enhance recovery from demyelination. In aged mice, metformin can restore responsiveness of oligodendrocyte progenitor cells (OPCs) to pro-differentiation cues, enhancing their ability to differentiate and thus repair myelin. However, metformin's influence on young oligodendroglia remains poorly understood. Here we investigated metformin's effect on the temporal dynamics of differentiation and metabolism in young, healthy oligodendroglia and in oligodendroglia following myelin damage in young adult mice. Our findings reveal that metformin accelerates early stages of myelin repair following cuprizone-induced myelin damage. Metformin treatment of both isolated OPCs and oligodendrocytes altered cellular bioenergetics, but in distinct ways,
Language	English
Publishing date	2023-10-12
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2452963-1
ISSN	1662-5102
ISSN	1662-5102
DOI	10.3389/fncel.2023.1254303
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Article ; Online: Distinct Requirements for Extracellular and Intracellular MMP12 in the Development of the Adult V-SVZ Neural Stem Cell Niche.

Shan, Xiwei / Tomlinson, Lyl / Yang, Qian / Colognato, Holly

Stem cell reports

2018 Volume 10, Issue 3, Page(s) 984–999

Abstract: The regulatory mechanisms that control neural stem cell (NSC) activation in the adult ventricular-subventricular zone (V-SVZ) stem cell niche have been the focus of intense investigation, yet how the niche first develops and organizes is poorly ... ...

Abstract	The regulatory mechanisms that control neural stem cell (NSC) activation in the adult ventricular-subventricular zone (V-SVZ) stem cell niche have been the focus of intense investigation, yet how the niche first develops and organizes is poorly understood. Here, we examined matrix metalloproteinases (MMPs) for potential roles in V-SVZ stem cell niche development. MMP12 was found to promote appropriate niche cellular arrangements, the formation of specialized niche extracellular matrix, and the translational planar cell polarity of ependymal cells that surround and support niche NSCs. Surprisingly, ependymal cells were found to have an intracellular pool of MMP12 that promoted ependymal cell ciliogenesis by upregulating FOXJ1. In addition, both extracellular and intracellular MMP12 were found to regulate V-SVZ niche output by promoting NSC quiescence. These findings reveal that extracellular and intracellular MMP12 have both unique and overlapping roles that help orchestrate the development of the adult V-SVZ stem cell niche.
MeSH term(s)	Animals ; Cell Polarity/physiology ; Ependyma/metabolism ; Ependyma/physiology ; Extracellular Matrix/metabolism ; Extracellular Matrix/physiology ; Forkhead Transcription Factors/metabolism ; Lateral Ventricles/metabolism ; Lateral Ventricles/physiology ; Matrix Metalloproteinase 12/metabolism ; Mice ; Mice, Inbred C57BL ; Neural Stem Cells/metabolism ; Neural Stem Cells/physiology ; Stem Cell Niche/physiology ; Up-Regulation/physiology
Chemical Substances	Forkhead Transcription Factors ; Matrix Metalloproteinase 12 (EC 3.4.24.65) ; matrix metallopeptidase 12, mouse (EC 3.4.24.65)
Language	English
Publishing date	2018-03-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	2720528-9
ISSN	2213-6711 ; 2213-6711
ISSN (online)	2213-6711
ISSN	2213-6711
DOI	10.1016/j.stemcr.2018.01.038
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Article ; Online: Prefrontal cortex NG2 glia undergo a developmental switch in their responsiveness to exercise.

Tomlinson, Lyl / Huang, Po Hsuan / Colognato, Holly

Developmental neurobiology

2018 Volume 78, Issue 7, Page(s) 687–700

Abstract: Aerobic exercise is known to influence brain function, e.g., enhancing executive function in both children and adults, with many of these influences being attributed to alterations in neurogenesis and neuronal function. Yet oligodendroglia in adult ... ...

Abstract	Aerobic exercise is known to influence brain function, e.g., enhancing executive function in both children and adults, with many of these influences being attributed to alterations in neurogenesis and neuronal function. Yet oligodendroglia in adult brains have also been reported to be highly responsive to exercise, including in the prefrontal cortex (PFC), a late myelinating region implicated in working memory. However, whether exercise affects oligodendroglia or myelination in juveniles, either in the PFC or in other brain regions, remains unknown. To address this, both juvenile and young adult mice were provided free access to running wheels for four weeks followed by an analysis of oligodendrocyte development and myelination in the PFC and the corpus callosum, a major white matter tract. Working memory and PFC NG2+ cell development were both affected by exercise in juvenile mice, yet surprisingly these exercise-mediated effects were distinct in juveniles and young adults. In the PFC, NG2+ cell proliferation was increased in exercising juveniles, but not young adults, whereas newly-born oligodendrocyte production was increased in exercising young adults, but not juveniles. Although no overall changes in myelin genes were found, elevated levels of Monocarboxylate Transporter 1, a glial lactate transporter important during active myelination, were found in the PFC of exercising young adults. Overall our findings reveal that long-term exercise modulates PFC glial development and does so differentially in juvenile and young adult mice, providing insight into the cellular responses that may underlie cognitive benefits to teenagers and young adults in response to exercise. © 2018 Wiley Periodicals, Inc. Develop Neurobiol 78: 687-700, 2018.
MeSH term(s)	Animals ; Antigens/metabolism ; Cell Proliferation/physiology ; Female ; Maze Learning/physiology ; Mice, Inbred C57BL ; Monocarboxylic Acid Transporters/metabolism ; Oligodendroglia/cytology ; Oligodendroglia/metabolism ; Prefrontal Cortex/cytology ; Prefrontal Cortex/growth & development ; Prefrontal Cortex/metabolism ; Proteoglycans/metabolism ; Running/physiology ; Running/psychology ; Symporters/metabolism
Chemical Substances	Antigens ; Monocarboxylic Acid Transporters ; Proteoglycans ; Symporters ; chondroitin sulfate proteoglycan 4 ; monocarboxylate transport protein 1
Language	English
Publishing date	2018-03-31
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2256184-5
ISSN	1932-846X ; 1097-4695 ; 1932-8451 ; 0022-3034
ISSN (online)	1932-846X ; 1097-4695
ISSN	1932-8451 ; 0022-3034
DOI	10.1002/dneu.22590
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Article ; Online: Myelination is delayed during postnatal brain development in the mdx mouse model of Duchenne muscular dystrophy.

Aranmolate, Azeez / Tse, Nathaniel / Colognato, Holly

BMC neuroscience

2017 Volume 18, Issue 1, Page(s) 63

Abstract: Background: In Duchenne muscular dystrophy (DMD), the loss of the dystrophin component of the dystrophin-glycoprotein complex (DGC) compromises plasma membrane integrity in skeletal muscle, resulting in extensive muscle degeneration. In addition, many ... ...

Abstract	Background: In Duchenne muscular dystrophy (DMD), the loss of the dystrophin component of the dystrophin-glycoprotein complex (DGC) compromises plasma membrane integrity in skeletal muscle, resulting in extensive muscle degeneration. In addition, many DMD patients exhibit brain deficits in which the cellular etiology remains poorly understood. We recently found that dystroglycan, a receptor component of the DGC that binds intracellularly to dystrophin, regulates the development of oligodendrocytes, the myelinating glial cells of the brain. Results: We investigated whether dystrophin contributes to oligodendroglial function and brain myelination. We found that oligodendrocytes express up to three dystrophin isoforms, in conjunction with classic DGC components, which are developmentally regulated during differentiation and in response to extracellular matrix engagement. We found that mdx mice, a model of DMD lacking expression of the largest dystrophin isoform, have delayed myelination and inappropriate oligodendrocyte progenitor proliferation in the cerebral cortex. When we prevented the expression of all oligodendroglial dystrophin isoforms in cultured oligodendrocytes using RNA interference, we found that later stages of oligodendrocyte maturation were significantly delayed, similar to mdx phenotypes in the developing brain. Conclusions: We find that dystrophin is expressed in oligodendrocytes and influences developmental myelination, which provides new insight into potential cellular contributors to brain dysfunction associated with DMD.
MeSH term(s)	Animals ; Brain/growth & development ; Brain/metabolism ; Brain/pathology ; Cells, Cultured ; Disease Models, Animal ; Female ; Gene Expression Regulation, Developmental ; Male ; Mice, Inbred C57BL ; Mice, Inbred mdx ; Muscular Dystrophy, Duchenne/metabolism ; Muscular Dystrophy, Duchenne/pathology ; Neural Stem Cells/metabolism ; Neural Stem Cells/pathology ; Oligodendroglia/metabolism ; Oligodendroglia/pathology ; Protein Isoforms ; RNA Interference ; RNA, Messenger/metabolism ; Rats, Sprague-Dawley
Chemical Substances	Protein Isoforms ; RNA, Messenger
Language	English
Publishing date	2017-08-14
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ISSN	1471-2202
ISSN (online)	1471-2202
DOI	10.1186/s12868-017-0381-0
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Article: The amniotic fluid-derived cells: the biomedical challenge for the third millennium.

Simoni, Giuseppe / Colognato, Renato

Journal of prenatal medicine

2012 Volume 3, Issue 3, Page(s) 34–36

Abstract: Human amniotic fluid cells (H-AFC) have been used as a diagnostic tool for the prenatal diagnosis ... of the Human amniotic fluid cells (H-AFC) the last but not least evidence, provided in the last 5 years ...

Abstract	Human amniotic fluid cells (H-AFC) have been used as a diagnostic tool for the prenatal diagnosis of fetal genetic anomalies for more than 50 years.In the early 1990s small nucleated cells, which were identified as he-matopoietic progenitors, were detected in the amniotic fluid. After this evidence several other scientific novelties as been brought out to the attention of the scientific community. In these brief history of the Human amniotic fluid cells (H-AFC) the last but not least evidence, provided in the last 5 years, suggests that they can also harbor a therapeutic potential for human diseases.
Language	English
Publishing date	2012-03-16
Publishing country	Italy
Document type	Journal Article
ZDB-ID	2658048-2
ISSN	1971-3290 ; 1971-3282
ISSN (online)	1971-3290
ISSN	1971-3282
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Article ; Online: Behavioral experiences as drivers of oligodendrocyte lineage dynamics and myelin plasticity.

Tomlinson, Lyl / Leiton, Cindy V / Colognato, Holly

Neuropharmacology

2015 Volume 110, Issue Pt B, Page(s) 548–562

Abstract: Many behavioral experiences are known to promote hippocampal neurogenesis. In contrast, the ability of behavioral experiences to influence the production of oligodendrocytes and myelin sheath formation remains relatively unknown. However, several recent ... ...

Abstract	Many behavioral experiences are known to promote hippocampal neurogenesis. In contrast, the ability of behavioral experiences to influence the production of oligodendrocytes and myelin sheath formation remains relatively unknown. However, several recent studies indicate that voluntary exercise and environmental enrichment can positively influence both oligodendrogenesis and myelination, and that, in contrast, social isolation can negatively influence myelination. In this review we summarize studies addressing the influence of behavioral experiences on oligodendrocyte lineage cells and myelin, and highlight potential mechanisms including experience-dependent neuronal activity, metabolites, and stress effectors, as well as both local and systemic secreted factors. Although more study is required to better understand the underlying mechanisms by which behavioral experiences regulate oligodendrocyte lineage cells, this exciting and newly emerging field has already revealed that oligodendrocytes and their progenitors are highly responsive to behavioral experiences and suggest the existence of a complex network of reciprocal interactions among oligodendrocyte lineage development, behavioral experiences, and brain function. Achieving a better understanding of these relationships may have profound implications for human health, and in particular, for our understanding of changes in brain function that occur in response to experiences. This article is part of the Special Issue entitled 'Oligodendrocytes in Health and Disease'.
MeSH term(s)	Animals ; Cell Differentiation ; Cell Plasticity/physiology ; Environment ; Exercise/physiology ; Humans ; Myelin Sheath/physiology ; Oligodendroglia/physiology ; Social Isolation ; Stem Cells/physiology
Language	English
Publishing date	2015-09-28
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	218272-5
ISSN	1873-7064 ; 0028-3908
ISSN (online)	1873-7064
ISSN	0028-3908
DOI	10.1016/j.neuropharm.2015.09.016
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