Multiple Sclerosis

Lee, Jae Young; Petratos, Steven

doi:10.1177/1073858413477207

Cited by 30 publications

(13 citation statements)

References 60 publications

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“…The biological meaning of this distinct expression pattern remains unknown, but it could influence disease pathogenesis and future therapeutic approaches. Indeed recent evidence supports the concept that targeting RTN4 signaling in MS could be a promising therapeutic approach (Lee and Petratos 2013). In fact, impairment of LINGO-1 or blockade of its pathway, as well as silencing of RTN4A, promoted functional recovery and limited clinical severity by stimulating axonal growth and repair in MOG 35–55 - and myelin basic protein-induced EAE models, ultimately improving the functional deficits caused by immune-mediated axonal damage (Mi et al 2007; Yang et al 2010).…”

Section: The Role Of Rtns In the Pathological Processes Of Neurodegenmentioning

confidence: 80%

The Role of Reticulons in Neurodegenerative Diseases

2013

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Reticulons (RTNs) are a group of membrane-associated proteins mainly responsible for shaping the tubular endoplasmic reticulum network, membrane trafficking, inhibition of axonal growth, and apoptosis. These proteins share a common sequence feature, the reticulon homology domain, which consists of paired hydrophobic stretches that are believed to induce membrane curvature by acting as a wedge in bilayer membranes. RTNs are ubiquitously expressed in all tissues, but each RTN member exhibits a unique expression pattern that prefers certain tissues or even cell types. Recently, accumulated evidence has suggested additional and unexpected roles for RTNs, including those on DNA binding, autophagy, and several inflammatory-related functions. These manifold actions of RTNs account for their ever-growing recognition of their involvement in neurodegenerative diseases like Alzheimer’s disease, amyotrophic lateral sclerosis, multiple sclerosis, as well as hereditary spastic paraplegia. This review summarizes the latest discoveries on RTNs in human pathophysiology, and the engagement of these in neurodegeneration, along with the implications of these findings for a better understanding of the molecular events triggered by RTNs and their potential exploitation as next-generation therapeutics.

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Section: The Role Of Rtns In the Pathological Processes Of Neurodegenmentioning

confidence: 80%

The Role of Reticulons in Neurodegenerative Diseases

2013

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“…The many gene products involved in Nogo-like signaling offer rich opportunities to target signaling, and, in particular, to inhibit signaling in order to improve axon regeneration and structural synaptic plasticity. This could be beneficial for human pathologies such as spinal cord injury, stroke, traumatic brain injury, multiple sclerosis, dementia, retinopathies, and developmental disturbances (Kim et al, 2004 ; Satoh et al, 2005 ; Fontoura and Steinman, 2006 ; Zhou et al, 2011 ; Lee and Petratos, 2013 ; Lindau et al, 2014 ; Liu et al, 2015 ; Sozmen et al, 2016 ; Pernet, 2017 ; Rodriguez et al, 2017 ). To help design such treatments, we need to know where the Nogo-like signaling genes are expressed, and how they are regulated together.…”

Section: Discussionmentioning

confidence: 99%

A Nogo-Like Signaling Perspective from Birth to Adulthood and in Old Age: Brain Expression Patterns of Ligands, Receptors and Modulators

Smedfors

Olson

Karlsson

2018

Front. Mol. Neurosci.

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An appropriate strength of Nogo-like signaling is important to maintain synaptic homeostasis in the CNS. Disturbances have been associated with schizophrenia, MS and other diseases. Blocking Nogo-like signaling may improve recovery after spinal cord injury, stroke and traumatic brain injury. To understand the interacting roles of an increasing number of ligands, receptors and modulators engaged in Nogo-like signaling, the transcriptional activity of these genes in the same brain areas from birth to old age in the normal brain is needed. Thus, we have quantitatively mapped the innate expression of 11 important genes engaged in Nogo-like signaling. Using in situ hybridization, we located and measured the amount of mRNA encoding Nogo-A, OMgp, NgR1, NgR2, NgR3, Lingo-1, Troy, Olfactomedin, LgI1, ADAM22, and MAG, in 18 different brain areas at six different ages (P0, 1, 2, 4, 14, and 104 weeks). We show gene- and area-specific activities and how the genes undergo dynamic regulation during postnatal development and become stable during adulthood. Hippocampal areas underwent the largest changes over time. We only found differences between individual cortical areas in Troy and MAG. Subcortical areas presented the largest inter-regional differences; lateral and basolateral amygdala had markedly higher expression than other subcortical areas. The widespread differences and unique expression patterns of the different genes involved in Nogo-like signaling suggest that the functional complexes could look vastly different in different areas.

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“…It is believed that neuronally differentiated P19 cells provide a good in vitro experimental model to study the presence and role of these Nogo binding partners and signaling molecules activated by Nogo-66. Recently, Nogo and NgR1 are also being studied for their possible involvement in CNS disorders or diseases, such as Alzheimer's disease, schizophrenia and multiple sclerosis [27,28,29]. We also believe that this P19 cell model could be an efficient tool to elucidate whether signaling events of Nogo and NgR1 interact with each other to perform any physiological functions, such as LTP or LTD (long-term depression) or participate in pathologic conditions of the CNS mentioned above.…”

Section: Discussionmentioning

confidence: 99%

NgR1 Expressed in P19 Embryonal Carcinoma Cells Differentiated by Retinoic Acid Can Activate STAT3

Lee

Yun

Baek

et al. 2015

Korean J Physiol Pharmacol

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NgR1, a Nogo receptor, is involved in inhibition of neurite outgrowth and axonal regeneration and regulation of synaptic plasticity. P19 embryonal carcinoma cells were induced to differentiate into neuron-like cells using all trans-retinoic acid and the presence and/or function of cellular molecules, such as NgR1, NMDA receptors and STAT3, were examined. Neuronally differentiated P19 cells expressed the mRNA and protein of NgR1, which could stimulate the phosphorylation of STAT3 when activated by Nogo-P4 peptide, an active segment of Nogo-66. During the whole period of differentiation, mRNAs of all of the NMDA receptor subtypes tested (NR1, NR2A-2D) were consistently expressed, which meant that neuronally differentiated P19 cells maintained some characteristics of neurons, especially central nervous system neurons. Our results suggests that neuronally differentiated P19 cells expressing NgR1 may be an efficient and convenient in vitro model for studying the molecular mechanism of cellular events that involve NgR1 and its binding partners, and for screening compounds that activate or inhibit NgR1.

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Multiple Sclerosis

Cited by 30 publications

References 60 publications

The Role of Reticulons in Neurodegenerative Diseases

The Role of Reticulons in Neurodegenerative Diseases

A Nogo-Like Signaling Perspective from Birth to Adulthood and in Old Age: Brain Expression Patterns of Ligands, Receptors and Modulators

NgR1 Expressed in P19 Embryonal Carcinoma Cells Differentiated by Retinoic Acid Can Activate STAT3

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