Increased autotaxin activity in multiple sclerosis

Zahednasab, Hamid; Balood, Mohammad; Harirchian, Mohammad Hossein; Mesbah‐Namin, Seyed Alireza; Rahimian, Nasrin; Siroos, Bahaadin

doi:10.1016/j.jneuroim.2014.06.006

Cited by 34 publications

(30 citation statements)

References 21 publications

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“…Related to prognostic marker for MS, it is well known that cortical atrophy is already present at the time of MS onset (15). Studies suggest that IL2A polymorphism might be associated with disease attacks (16)(17)(18)(19). Another study proposed that switch-associated protein 70 antibodies could be involved in MS relapse (20).…”

Section: Discussionmentioning

confidence: 99%

Demographic Analysis of Patients With Multiple Sclerosis; Individual Variability Related to the Time Interval

Tolou-Ghamari

2015

Arch Neurosci

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Background: According to the published articles, there is an increase in the prevalence of MS all over the world. Regarding demographic characteristics for unknown reasons, females are more affected than males. Objectives: The aim of this study was demographic analysis and model of changes in patients for three years in a local teaching hospital in Isfahan/Iran. Results: Of the total population studied, 75% were female. 32% and 33% of patients related to the age groups of 20 -30 and 30 -40 years, respectively. However the number of patients related to time interval I3 were 472, but there was an increase in the number of patients studied from I1 to I2 (394 vs. 634). Approximately 13% of total population had MS attack more than 4 to 19 times. Conclusions:In agreement with previous reports, due to unknown reasons, the number of patients in general and the number of females in particular were increased annually. Within this population due to inter-and intra-individual variability, pharmacokinetic studies seem to be valuable.

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Section: Discussionmentioning

confidence: 99%

Demographic Analysis of Patients With Multiple Sclerosis; Individual Variability Related to the Time Interval

Tolou-Ghamari

2015

Arch Neurosci

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“…In the CNS, ATX-dependent LPA signaling has been suggested to participate in initiation of neuropathic pain [4,11], while increased ATX expression has been reported in neuroblastomas and glioblastomas [12]. Deregulated ATX and LPA levels have been reported, with some controversy, in the sera and cerebrospinal fluid (CSF) of patients with multiple sclerosis (MS) [13][14][15][16][17], as well as in mice with experimental autoimmune encephalomyelitis (EAE) [17,18], suggesting a role for ATX/LPA in the pathogenesis of MS/EAE. Moreover, pharmacologic potent ATX inhibition has been reported to attenuate the development of EAE [19], further suggesting potential therapeutic benefits in targeting ATX in MS.…”

Section: Introductionmentioning

confidence: 99%

ATX expression from GFAP⁺cells is essential for embryonic development

Sevastou

Ninou

Aidinis

2020

Preprint

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Autotaxin (ATX) is secreted by various type of cells in health and disease and catalyzes the extracellular production of lysophosphatidic acid (LPA). In turn, LPA is a bioactive lysophospholipid promoting a wide array of cellular functions through its multiple Gprotein coupled receptors, differentially expressed in almost all cell types. ATX expression has been shown necessary for embryonic development and has been suggested to participate in the pathogenesis of different chronic inflammatory diseases and cancer. Deregulated ATX and LPA levels have been reported in multiple sclerosis (MS) and its experimental model, experimental autoimmune encephalomyelitis (EAE). ATX genetic deletion from macrophages and microglia (CD11b + cells) attenuated the severity of EAE, thus proposing a pathogenic role for the ATX/LPA axis in MS/EAE. In this report, increased ATX staining was localized to glial fibrillary acidic protein positive (GFAP + ) cells, mostly astrocytes, in spinal cord sections from EAE mice at the peak of the disease. However, genetic deletion of ATX from GFAP + cells resulted in embryonic lethality, suggesting a major role for ΑΤΧ expression from GFAP + cells in embryonic development, that urges further dissection. Moreover, the re-expression of ATX from GFAP+ cells during the pathogenesis of EAE, reinforces the concept that ATX/LPA is a developmental program aberrantly reactivated upon chronic inflammation.

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“…Thus, ATX likely represents a permissive/promotional cue that is limited in the CNS parenchyma under pathological conditions of inefficient myelin regeneration. It is of note, however, that contrary to the CNS parenchyma, ATX protein levels in the cerebrospinal fluid of relapsing-remitting MS patients appear increased likely due to functional roles related to the pro-inflammatory environment (Hammack et al, 2004; Zahednasab et al, 2014). Toward the development of promising therapeutic approaches enhancing remyelination, it seems thus necessary to design strategies specifically targeting the signaling axis that is initiated by ATX in the CNS parenchyma and directed at cells of the OLG lineage.…”

Section: Introductionmentioning

confidence: 99%

Extracellular cues influencing oligodendrocyte differentiation and (re)myelination

Wheeler

Fuss

2016

Experimental Neurology

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There is an increasing number of neurologic disorders found to be associated with loss and/or dysfunction of the CNS myelin sheath, ranging from the classic demyelinating disease, Multiple Sclerosis, through CNS injury, to neuropsychiatric diseases. The disabling burden of these diseases has sparked a growing interest in gaining a better understanding of the molecular mechanisms regulating the differentiation of the myelinating cells of the CNS, oligodendrocytes (OLGs), and the process of (re)myelination. In this context, the importance of the extracellular milieu is becoming increasingly recognized. Under pathological conditions, changes in inhibitory as well as permissive/promotional cues are thought to lead to an overall extracellular environment that is obstructive for the regeneration of the myelin sheath. Given the general view that remyelination is, even though limited in human, a natural response to demyelination, targeting pathologically ‘dysregulated’ extracellular cues and their downstream pathways is regarded as a promising approach toward the enhancement of remyelination by endogenous (or if necessary transplanted) OLG progenitor cells. In this review, we will introduce the extracellular cues that have been implicated in the modulation of (re)myelination. These cues can be soluble, part of the extracellular matrix (ECM) or mediators of cell-cell interactions. Their inhibitory and permissive/promotional roles with regard to remyelination as well as their potential for therapeutic intervention will be discussed.

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Increased autotaxin activity in multiple sclerosis

Cited by 34 publications

References 21 publications

Demographic Analysis of Patients With Multiple Sclerosis; Individual Variability Related to the Time Interval

Demographic Analysis of Patients With Multiple Sclerosis; Individual Variability Related to the Time Interval

ATX expression from GFAP⁺cells is essential for embryonic development

Extracellular cues influencing oligodendrocyte differentiation and (re)myelination

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Increased autotaxin activity in multiple sclerosis

Cited by 34 publications

References 21 publications

Demographic Analysis of Patients With Multiple Sclerosis; Individual Variability Related to the Time Interval

Demographic Analysis of Patients With Multiple Sclerosis; Individual Variability Related to the Time Interval

ATX expression from GFAP+cells is essential for embryonic development

Extracellular cues influencing oligodendrocyte differentiation and (re)myelination

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Product

Resources

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ATX expression from GFAP⁺cells is essential for embryonic development