Modelos experimentales de desmielinización-remielinización

Torre-Fuentes, Laura; Moreno-Jiménez, Lidia; Pytel, Vanesa; Matías‐Guiu, Jordi A.; Gómez‐Pinedo, Ulises

doi:10.1016/j.nrl.2017.07.002

Cited by 26 publications

(10 citation statements)

References 52 publications

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“…EtBr is a DNA intercalator and its toxicity preferentially impacts astrocytes by restricting their ability to release trophic factors leading to associated OLs to die, along with the affected astrocytes, while largely sparing neurons. The death of these glia in and around the injection site results in localized demyelination (Torre-Fuentes et al, 2020 ). Immunoreactive GFAP + astrocytes are then recruited, but remain confined to the lesion perimeter.…”

Section: Murine Models Of Msmentioning

confidence: 99%

“…Interestingly, while demyelination has been described as being T and B cell-independent, CD4- and CD8-deficient mice had significantly reduced remyelination at the injection site compared to controls, indicating T cells may be involved in myelin repair and proper OPC function (Bieber et al, 2003 ). Unlike EtBr and CPZ, lysolecithin is not considered to be fully immune-independent, acting as a chemoattractant to monocytes and initiating a limited focal inflammatory response (Torre-Fuentes et al, 2020 ) and remyelination that is accompanied by significant astrogliosis (Jeffery and Blakemore, 1995 ). While useful, EtBr and lysolecithin are technically demanding models and de- and remyelination is restricted to the site of injection.…”

Section: Murine Models Of Msmentioning

confidence: 99%

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Connecting Neuroinflammation and Neurodegeneration in Multiple Sclerosis: Are Oligodendrocyte Precursor Cells a Nexus of Disease?

Psenicka

Smith

Tinkey

et al. 2021

Front. Cell. Neurosci.

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The pathology in neurodegenerative diseases is often accompanied by inflammation. It is well-known that many cells within the central nervous system (CNS) also contribute to ongoing neuroinflammation, which can promote neurodegeneration. Multiple sclerosis (MS) is both an inflammatory and neurodegenerative disease in which there is a complex interplay between resident CNS cells to mediate myelin and axonal damage, and this communication network can vary depending on the subtype and chronicity of disease. Oligodendrocytes, the myelinating cell of the CNS, and their precursors, oligodendrocyte precursor cells (OPCs), are often thought of as the targets of autoimmune pathology during MS and in several animal models of MS; however, there is emerging evidence that OPCs actively contribute to inflammation that directly and indirectly contributes to neurodegeneration. Here we discuss several contributors to MS disease progression starting with lesion pathology and murine models amenable to studying particular aspects of disease. We then review how OPCs themselves can play an active role in promoting neuroinflammation and neurodegeneration, and how other resident CNS cells including microglia, astrocytes, and neurons can impact OPC function. Further, we outline the very complex and pleiotropic role(s) of several inflammatory cytokines and other secreted factors classically described as solely deleterious during MS and its animal models, but in fact, have many neuroprotective functions and promote a return to homeostasis, in part via modulation of OPC function. Finally, since MS affects patients from the onset of disease throughout their lifespan, we discuss the impact of aging on OPC function and CNS recovery. It is becoming clear that OPCs are not simply a bystander during MS progression and uncovering the active roles they play during different stages of disease will help uncover potential new avenues for therapeutic intervention.

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Section: Murine Models Of Msmentioning

confidence: 99%

Section: Murine Models Of Msmentioning

confidence: 99%

Connecting Neuroinflammation and Neurodegeneration in Multiple Sclerosis: Are Oligodendrocyte Precursor Cells a Nexus of Disease?

Psenicka

Smith

Tinkey

et al. 2021

Front. Cell. Neurosci.

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“…SFV is an enveloped virus with the capability of entering CNS and subsequently causing myelin damage (Torre-Fuentes et al, 2017).…”

Section: Semliki Forest Virusmentioning

confidence: 99%

“…Hosts usually recover from this initial period and during the following 4 weeks, a chronic phase can be recognized, defined as a neuroparalytic disease with demyelinating inflammatory lesions similar to MS (Houtman & Fleming, 1996;Lane & Buchmeier, 1997;Steinman, 1996;Torre-Fuentes et al, 2017). At this point, MHV titers are below detection limits and T cells and macrophages are considered the main effectors of demyelination (Wu, Dandekar, Pewe, & Perlman, 2000).…”

Section: Mouse Hepatitis Virus (Mhv)mentioning

confidence: 99%

Biological models in multiple sclerosis

Sanabria-Castro

Flores-Dı́az

Alape-Girón

2019

J of Neuroscience Research

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Considering the etiology of multiple sclerosis (MS) is still unknown, experimental models resembling specific aspects of this immune‐mediated demyelinating human disease have been developed to increase the understanding of processes related to pathogenesis, disease evolution, evaluation of therapeutic interventions, and demyelination and remyelination mechanisms. Based on the nature of the investigation, biological models may include in vitro, in vivo, and ex vivo assessments. Even though these approaches have disclosed valuable information, every disease animal model has limitations and can only replicate specific features of MS. In vitro and ex vivo models generally do not reflect what occurs in the organism, and in vivo animal models are more likely used; nevertheless, they are able to reproduce only certain stages of the disease. In vivo MS disease animal models in mammals include: experimental autoimmune encephalomyelitis, viral encephalomyelitis, and induced demyelination. This review examines and describes the most common biological disease animal models for the study of MS, their specific characteristics and limitations.

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“…EAE is a suitable model, in which animals develop inflammatory-demyelinating diseases spontaneously and cover the specific spectrum of the pathological and immunological features of MS (Lassmann and Bradl, 2017 ). In mice, the EAE-ON model is induced by injection of myelin oligodendrocyte glycoprotein (MOG) peptide-MOG35–55, and clinical EAE scores are graded daily and blindly according to the standard scoring system (Dietrich et al, 2018 ; Locri et al, 2018 ; Torre-Fuentes et al, 2020 ). Our previous results showed that retinal ganglion cells (RGC), in the retina, were most affected by ON (Huang et al, 2017 ).…”

Section: Introductionmentioning

confidence: 99%

Effects of Retinal Transcription Regulation After GB20 Needling Treatment in Retina With Optic Neuritis

Chen

Zhang

Gan

et al. 2020

Front. Integr. Neurosci.

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Optic neuritis (ON) is one of the most frequent symptoms of multiple sclerosis (MS) that results in progressive loss of axons and neurons. In clinical trials of Traditional Chinese Medicine, needling at the GB20 acupoint has been widely used for the treatment of ocular diseases, including ON. However, the molecular mechanisms of needling at this site are still unclear. In this study, we generated an experimental autoimmune encephalomyelitis (EAE) mouse model and investigated the effects of needling treatment at the GB20 acupoint on retina with EAE-associated ON. RNA sequencing of the retinal transcriptome revealed that, of the 234 differentially expressed genes induced by ON, 100 genes were upregulated, and 134 genes were downregulated by ON, while needling at the GB20 acupoint specifically reversed the expression of 21 genes compared with control treatment at GV16 acupoint. Among the reversed genes, Nr4a3, Sncg, Uchl1, and Tppp3 were involved in axon development and regeneration and were downregulated by ON, indicating the beneficial effect of needling at GB20. Further gene ontology (GO) enrichment analysis revealed that needling at GB20 affected the molecular process of Circadian rhythm in mouse retina with ON. Our study first reported that needling treatment after ON at the GB20 acupoint regulated gene expression of the retina and reversed the expression of downregulated axon development-related genes. This study also demonstrated that GV16 was a perfect control treatment site for GB20 in animal research. Our study provided a scientific basis for needling treatments at GB20 for ocular diseases.

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Modelos experimentales de desmielinización-remielinización

Abstract: Experimental models provide a deeper understanding of the different pathogenic mechanisms involved in multiple sclerosis. Choosing one model or another depends on the specific aims of the study.

Cited by 26 publications

References 52 publications

Connecting Neuroinflammation and Neurodegeneration in Multiple Sclerosis: Are Oligodendrocyte Precursor Cells a Nexus of Disease?

Connecting Neuroinflammation and Neurodegeneration in Multiple Sclerosis: Are Oligodendrocyte Precursor Cells a Nexus of Disease?

Biological models in multiple sclerosis

Effects of Retinal Transcription Regulation After GB20 Needling Treatment in Retina With Optic Neuritis

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