Osteopontin and multiple sclerosis: An update

Niino, Masaaki; Kikuchi, Seiji

doi:10.1111/j.1759-1961.2011.00019.x

Cited by 12 publications

(6 citation statements)

References 68 publications

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“…MS patients have higher levels of osteopontin (OPN) in serum and cerebrospinal fluid (CSF). OPN is produced by T cells, B cells, macrophages, NK cells, dendritic cells, and neutrophils and acts as a pro-inflammatory cytokine by inducing the production of IL-12 in macrophages and IFN-γ in T cells and inhibition of IL-10 production in macrophages ( Niino and Kikuchi, 2011 ). Also, increased IFN-γ and IL-12 lead to the upregulation of Th1 cells in the brain ( Khaibullin et al, 2017 ).…”

Section: Introductionmentioning

confidence: 99%

Multisystem Inflammatory Syndrome and Autoimmune Diseases Following COVID-19: Molecular Mechanisms and Therapeutic Opportunities

Hosseini

Fallahi

Erabi

et al. 2022

Front. Mol. Biosci.

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Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2), has led to huge concern worldwide. Some SARS-CoV-2 infected patients may experience post–COVID-19 complications such as multisystem inflammatory syndrome, defined by symptoms including fever and elevated inflammatory markers (such as elevation of C reactive protein (CRP), erythrocyte sedimentation rate, fibrinogen, procalcitonin test, D-dimer, ferritin, lactate dehydrogenase or IL-6, presence of neutrophilia, lymphopenia, decreased albumin, and multiple organ dysfunction). Post–COVID-19 complications may also manifest as autoimmune diseases such as Guillain-Barré syndrome and systemic lupus erythematosus. Signaling disorders, increased inflammatory cytokines secretion, corticosteroid use to treat COVID-19 patients, or impaired immune responses are suggested causes of autoimmune diseases in these patients. In this review, we discuss the molecular and pathophysiological mechanisms and therapeutic opportunities for multisystem inflammatory syndrome and autoimmune diseases following SARS-CoV-2 infection with the aim to provide a clear view for health care providers and researchers.

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Section: Introductionmentioning

confidence: 99%

Multisystem Inflammatory Syndrome and Autoimmune Diseases Following COVID-19: Molecular Mechanisms and Therapeutic Opportunities

Hosseini

Fallahi

Erabi

et al. 2022

Front. Mol. Biosci.

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“…Until recently, research on OPN has focused on its pathophysiological role. In particular, OPN is considered as an inflammatory mediator in various neurodegenerative diseases such as multiple sclerosis [11,12], Alzheimer’s disease [13], and Parkinson’s disease [14]. However, importantly, Jiang et al [15] recently described the functional role of OPN in brain development.…”

Section: Introductionmentioning

confidence: 99%

Effects of Ascorbic Acid on Osteopontin Expression and Axonal Myelination in the Developing Cerebellum of Lead-Exposed Rat Pups

Nam

Seo

Nahm

et al. 2019

IJERPH

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Osteopontin (OPN) is a multi-functional protein that binds to integrin and calcium-binding phosphoprotein. OPN is required for normal neuronal development and its axonal myelination. We studied the combined effect of lead (Pb) and ascorbic acid treatment on OPN expression in the developing cerebellum. We randomly divided pregnant female rats into three groups: control, Pb (lead acetate, 0.3%, drinking water), and Pb plus ascorbic acid (PA; ascorbic acid, 100 mg/kg, oral intubation) groups. The blood level of Pb was significantly increased, while ascorbic acid reduced Pb levels in the dams and pups. At postnatal day (PND) 21, results from Nissl staining and OPN immunohistochemistry demonstrated that OPN was detected in the Purkinje cell layer in the cerebellum. Ascorbic acid treatment mitigated Pb exposure-induced reduction in the number of intact Purkinje cells and OPN immunoreactive Purkinje cells in the cerebellum of pups. In addition, Pb-induced reduction in the number of oligodendrocytes and myelin-associated glycoprotein is associated with the malformation of the myelin sheath. Ascorbic acid provided protection from Pb-induced impairments. Pb-induced structural deficits in the cerebellum resulted in functional deterioration observed during locomotive tests (bar holding test and wire mesh ascending test), while ascorbic acid ameliorated these harmful effects. Present results suggest that the change of OPN is associated with myelination in the developing cerebellum. The results also demonstrated that exposure to Pb is harmful, while ascorbic acid treatment is beneficial.

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“…OPN is widely expressed in neurons of the developing and adult brain (Shin et al, 1999 ; Lee et al, 2001 ; Iczkiewicz et al, 2004 ), but its endogenous functions remain unknown. In the pathological brain, OPN is implicated as a mediator of pro-inflammatory effects in a variety of neurodegenerative diseases such as multiple sclerosis (Kim et al, 2004 ; Hur et al, 2007 ; Niino and Kikuchi, 2011 ), Alzheimer’s disease (Wung et al, 2007 ; Comi et al, 2010 ; Wirths et al, 2010 ), Parkinson’s disease (Iczkiewicz et al, 2006 ; Mattson et al, 2008 ), and ischemic stroke (Ellison et al, 1998 ; Wang et al, 1998 ; Schroeter et al, 2006 ; Choi et al, 2007 ). Specifically, OPN is secreted by macrophages, activated microglia, and astrocytes, and is generally thought to promote the inflammatory activation of microglia and macrophage infiltration (Kim et al, 2004 ; Schroeter et al, 2006 ; Choi et al, 2007 ; Wirths et al, 2010 ).…”

Section: Introductionmentioning

confidence: 99%

Increased Expression of Osteopontin in Retinal Degeneration Induced by Blue Light-Emitting Diode Exposure in Mice

Chang

Kim

et al. 2016

Front. Mol. Neurosci.

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Osteopontin (OPN) is a multifunctional adhesive glycoprotein that is implicated in a variety of pro-inflammatory as well as neuroprotective and repair-promoting effects in the brain. As a first step towards understanding the role of OPN in retinal degeneration (RD), we examined changes in OPN expression in a mouse model of RD induced by exposure to a blue light-emitting diode (LED). RD was induced in BALB/c mice by exposure to a blue LED (460 nm) for 2 h. Apoptotic cell death was evaluated by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. In order to investigate changes in OPN in RD, western blotting and immunohistochemistry were performed. Anti-OPN labeling was compared to that of anti-glial fibrillary acidic protein (GFAP), which is a commonly used marker for retinal injury or stress including inflammation. OPN expression in RD retinas markedly increased at 24 h after exposure, was sustained through 72 h, and subsided at 120 h. Increased OPN expression was observed co-localized with microglial cells in the outer nuclear layer (ONL), outer plexiform layer (OPL), and subretinal space. Expression was restricted to the central retina in which photoreceptor cell death occurred. Interestingly, OPN expression in the ONL/OPL was closely associated with microglia, whereas most of the OPN plaques observed in the subretinal space were not. Immunogold electron microscopy demonstrated that OPN was distributed throughout the cytoplasm of microglia and in nearby fragments of degenerating photoreceptors. In addition, we found that OPN was induced more acutely and with greater region specificity than GFAP. These results indicate that OPN may be a more useful marker for retinal injury or stress, and furthermore act as a microglial pro-inflammatory mediator and a phagocytosis-inducing opsonin in the subretinal space. Taken together, our data suggest that OPN plays an important role in the pathogenesis of RD.

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Osteopontin and multiple sclerosis: An update

Cited by 12 publications

References 68 publications

Multisystem Inflammatory Syndrome and Autoimmune Diseases Following COVID-19: Molecular Mechanisms and Therapeutic Opportunities

Multisystem Inflammatory Syndrome and Autoimmune Diseases Following COVID-19: Molecular Mechanisms and Therapeutic Opportunities

Effects of Ascorbic Acid on Osteopontin Expression and Axonal Myelination in the Developing Cerebellum of Lead-Exposed Rat Pups

Increased Expression of Osteopontin in Retinal Degeneration Induced by Blue Light-Emitting Diode Exposure in Mice

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