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  • 1
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    Online Resource
    Cystatin C induces apoptosis and tyrosine hydroxylase gene expression through JNK-dependent pathway in neuronal cells
    Elsevier BV ; 2011
    In:  Neuroscience Letters Vol. 496, No. 2 ( 2011-6), p. 100-105
    Details
    In: Neuroscience Letters, Elsevier BV, Vol. 496, No. 2 ( 2011-6), p. 100-105
    Type of Medium: Online Resource
    ISSN: 0304-3940
    URL: Article
    DOI: 10.1016/j.neulet.2011.03.091
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2011
    detail.hit.zdb_id: 1498535-4
    SSG: 12
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  • 2
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    Transplantation of a bone marrow mesenchymal stem cell line increases neuronal progenitor cell migration in a cerebral ischemia animal model
    Springer Science and Business Media LLC ; 2018
    In:  Scientific Reports Vol. 8, No. 1 ( 2018-10-08)
    Details
    In: Scientific Reports, Springer Science and Business Media LLC, Vol. 8, No. 1 ( 2018-10-08)
    Abstract: Mesenchymal stem cell (MSC) transplantation is demonstrated to improve functional and pathological recovery in cerebral ischemia. To understand the underlying mechanism, we transplanted a MSC line (B10) in a rat middle cerebral artery occlusion (MCAO) model and checked the proliferation and migration of neuronal progenitor cells (NPCs). B10 transplantation increased NPCs in the subventricular zone and their migration towards the lesion area at an earlier time. Fourteen days after MCAO, some NPCs were differentiated to neurons and astrocytes. Although B10 transplantation increased total number of both astrocytes and neurons, it only increased the differentiation of NPC to astrocyte. The mRNA of polysialylation enzyme ST8SiaIV and a chemokine SDF-1 were persistently increased in B10-transplanted groups. SDF-1-positive cell number was increased in the core and penumbra area, which was expressed in macrophage/microglia and transplanted B10 cells at 3 days after MCAO. Furthermore, SDF-1 mRNA expression in cell culture was high in B10 compared to a microglia (HMO) or a neuronal (A1) cell line. B10 culture supernatant increased in vitro A1 cell migration, which was significantly inhibited by siRNA-mediated SDF-1 silencing in B10. Thus, our results suggested that MSC transplantation increased endogenous NPC migration in cerebral ischemic condition by increasing chemokine and polysialylation enzyme expression, which could be helpful for the restorative management of cerebral ischemia.
    Type of Medium: Online Resource
    ISSN: 2045-2322
    URL: Article
    DOI: 10.1038/s41598-018-33030-9
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2018
    detail.hit.zdb_id: 2615211-3
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  • 3
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    A human neural stem cell line provides neuroprotection and improves neurological performance by early intervention of neuroinflammatory system
    Elsevier BV ; 2016
    In:  Brain Research Vol. 1631 ( 2016-01), p. 194-203
    Details
    In: Brain Research, Elsevier BV, Vol. 1631 ( 2016-01), p. 194-203
    Type of Medium: Online Resource
    ISSN: 0006-8993
    URL: Article
    DOI: 10.1016/j.brainres.2015.11.031
    RVK:
    XA 10000
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2016
    detail.hit.zdb_id: 1462674-3
    SSG: 12
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  • 4
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    Association between cystatin C gene polymorphism and the prevalence of white matter lesion in elderly healthy subjects
    Springer Science and Business Media LLC ; 2020
    In:  Scientific Reports Vol. 10, No. 1 ( 2020-03-13)
    Details
    In: Scientific Reports, Springer Science and Business Media LLC, Vol. 10, No. 1 ( 2020-03-13)
    Abstract: Cystatin C (CST3) is a cysteine protease inhibitor abundant in the central nervous system, and demonstrated to have roles in several pathophysiological processes including vascular remodeling and inflammation. Previously, we showed a relation of CST3 gene polymorphisms with deep and subcortical white matter hyperintensity (DSWMH) in a small case-control study. In this study, we aimed to investigate the relation in a larger cross-sectional study. Participants of a brain health examination program were recruited (n = 1795) in the study, who underwent routine blood tests and cognitive function tests. Cerebral white matter changes were analyzed by MRI. Additionally, 7 single nucleotide polymorphisms (SNPs) (−82G/C, −78T/G, −5G/A, +4A/C, +87C/T, +148G/A and +213G/A) in the promoter and coding regions of CST3 gene were examined. Among them, carriers of the minor allele haplotype −82C/+4C/+148A were significantly associated with decreased CST3 concentration in the plasma. Unadjusted analysis did not show significant relation between carriers of the minor allele haplotype and periventricular hyperintensity (PVH), but DSWMH was marginally ( p   〈  0.054) increased in this group. After adjusting the effects of other variables like age and kidney function, logistic regression analysis revealed that carriers of the minor allele haplotype were at a significantly increased risk of developing both PVH and DSWMH. Thus, our results suggest that carriers of the minor allele haplotype −82C/+4C/+148A of CST3 gene could be at an increased risk to develop cerebral white matter disturbance.
    Type of Medium: Online Resource
    ISSN: 2045-2322
    URL: Article
    DOI: 10.1038/s41598-020-61383-7
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2020
    detail.hit.zdb_id: 2615211-3
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  • 5
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    A Mesenchymal stem cell line (B10) increases angiogenesis in a rat MCAO model
    Elsevier BV ; 2019
    In:  Experimental Neurology Vol. 311 ( 2019-01), p. 182-193
    Details
    In: Experimental Neurology, Elsevier BV, Vol. 311 ( 2019-01), p. 182-193
    Type of Medium: Online Resource
    ISSN: 0014-4886
    URL: Article
    DOI: 10.1016/j.expneurol.2018.10.001
    RVK:
    XA 10000
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2019
    detail.hit.zdb_id: 1466932-8
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  • 6
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    Proteomic analysis of extracellular vesicles enriched serum associated with future ischemic stroke
    Springer Science and Business Media LLC ; 2021
    In:  Scientific Reports Vol. 11, No. 1 ( 2021-12-15)
    Details
    In: Scientific Reports, Springer Science and Business Media LLC, Vol. 11, No. 1 ( 2021-12-15)
    Abstract: Identifying new biomarkers beyond the established risk factors that make it possible to predict and prevent ischemic stroke has great significance. Extracellular vesicles are powerful cell‒cell messengers, containing disease-specific biomolecules, which makes them powerful diagnostic candidates. Therefore, this study aimed to identify proteins derived from extracellular vesicles enriched serum related to future ischemic stroke events, using a proteomic method. Of Japanese subjects who voluntarily participated in health checkups at our institute a number of times, 10 subjects (6 males and 4 females, age: 64.2 ± 3.9 years) who developed symptomatic ischemic stroke (7.3 ± 4.4 years’ follow-up) and 10 age‒sex matched controls without brain lesions (6.7 ± 2.8 years’ follow-up) were investigated. Extracellular vesicles enriched fractions were derived from serum collected at the baseline visit. Differentially expressed proteins were evaluated using isobaric tagging for relative and absolute protein quantification (iTRAQ)-based proteomic analysis. Of the 29 proteins identified, alpha-2-macroglobulin, complement C1q subcomponent subunit B, complement C1r subcomponent, and histidine-rich glycoprotein were significantly upregulated (2.21-, 2.15-, 2.24-, and 2.16-fold, respectively) in subjects with future ischemic stroke, as compared with controls. Our study supports the concept of serum-derived extracellular vesicles enriched fractions as biomarkers for new-onset stroke. These proteins may be useful for prediction or for targeted therapy.
    Type of Medium: Online Resource
    ISSN: 2045-2322
    URL: Article
    DOI: 10.1038/s41598-021-03497-0
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2021
    detail.hit.zdb_id: 2615211-3
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  • 7
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    Human mesenchymal stem cell transplantation changes proinflammatory gene expression through a nuclear factor‐κB‐dependent pathway in a rat focal cerebral ischemic model
    Wiley ; 2013
    In:  Journal of Neuroscience Research Vol. 91, No. 11 ( 2013-11), p. 1440-1449
    Details
    In: Journal of Neuroscience Research, Wiley, Vol. 91, No. 11 ( 2013-11), p. 1440-1449
    Abstract: Previous studies have demonstrated the immunomodulatory functions of mesenchymal stem cells (MSCs) in cerebral ischemic rats. However, the underlying mechanisms are unclear. The purpose of this study is to investigate the effects of MSC transplantation on transcriptional regulations of proinflammatory genes in cerebral ischemia. Transient ischemia was induced by middle cerebral artery occlusion (MCAO) in adult male Sprague‐Dawley rats. After 24 hr, vehicle (PBS) or a human MSC line (B10) was transplanted intravenously. The neurological deficits, infarct volume, cellular accumulations, and gene expression changes were monitored by means of behavior tests, MRI, immunohistochemistry, Western blotting, laser capture microdissection, and real‐time PCR. In the core area of the B10 transplantation group, the number of ED1‐positive macrophage/microglia was decreased compared with the PBS group. In the core, nuclear factor‐κB (NF‐κB) was decreased, although CCAAT/enhancer‐binding protein β was not changed; both were expressed mainly in ED1‐positive macrophage/microglia. Likewise, mRNAs of NF‐κB‐dependent genes including interleukin‐1β, MCP‐1, and inducible nitric oxide synthase were decreased in ED1‐positive and Iba‐1‐positive macrophage/microglia in the B10 transplantation group. Moreover, upstream receptors of the NF‐κB pathway, including CD40 and Toll‐like receptor 2 (TLR2), were decreased. Immunofluorescence results showed that, in the B10 transplantation group, the percentages of NF‐κB‐positive, CD40‐positive, and TLR2‐positive cells were decreased in ED1‐positive macrophage/microglia. Furthermore, NF‐κB‐positive cells in the CD40‐ or TLR2‐expressing cell population were decreased in the B10 transplantation group. This study demonstrates that B10 transplantation inhibits NF‐κB activation, possibly through inhibition of CD40 and TLR2, which might be responsible for the inhibition of proinflammatory gene expression in macrophage/microglia in the infarct lesion. © 2013 Wiley Periodicals, Inc.
    Type of Medium: Online Resource
    ISSN: 0360-4012 , 1097-4547
    URL: Issue
    URL: Article
    DOI: 10.1002/jnr.v91.11
    DOI: 10.1002/jnr.23267
    Language: English
    Publisher: Wiley
    Publication Date: 2013
    detail.hit.zdb_id: 1474904-X
    SSG: 12
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  • 8
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    Abstract 2513: Intraventricular Administration of Cystatin C Attenuates White Matter Injury In Rat Chronic Ischemia
    Ovid Technologies (Wolters Kluwer Health) ; 2012
    In:  Stroke Vol. 43, No. suppl_1 ( 2012-02)
    Details
    In: Stroke, Ovid Technologies (Wolters Kluwer Health), Vol. 43, No. suppl_1 ( 2012-02)
    Abstract: Background and Purpose Cerebral white matter lesions (WMLs) contribute to elderly cognitive deterioration and are usually caused by chronic ischemic insult. Experimental studies have shown that proteases are highly expressed in activated astrocyte and microglia, which are thought to be crucial in the development of WMLs. Cystatin C (CSTC) functions as a major extracellular cysteine protease inhibitor in mammals. Since the concentration of CSTC is 5 times higher in CSF than in plasma, CSTC is thought to be a major inhibitor of cysteine proteases in the central nervous system. We have shown that polymorphisms in the CSTC gene, which results in a decrease of plasma CSTC level, are significantly associated with prevalence of WMLs. However, direct impact of CSTC on the development of WMLs has not been elucidated yet. Here we studied whether direct administration of CSTC into brain has a protective effect on the pathophysiology of WMLs produced by chronic cerebral hypoperfusion in a rat model of permanent bilateral common carotid artery occlusion. Methods Adult Wister rats underwent ligation of bilateral common carotid arteries (LBCCA) and were divided into three groups; the CSTC group in which CSTC was injected continuously into the ventricle 14 consecutive days after LBCCA (n=10), the PBS group in which PBS was injected continuously into the ventricle 14 consecutive days after LBCCA (n=10), and the sham group (n=10). All rats were perfused on 14 days after LBCCA. The severity of WMLs and accumulation of microglia and astrocytes in the corpus callosum (CC) and optic nerve (ON) were evaluated. Furthermore, the activity of cathepsin B, one of the major proteases, was measured in the tissue lysates of CC and ON using the assay kit. Results Continuous intraventricular infusion of CSTC significantly reduced the severity of WMLs (CC; p 〈 0.001 vs. PBS, ON; p 〈 0.001 vs. PBS) and inhibited the accumulation and activation of microglia (CC; p=0.03 vs. PBS, ON; p 〈 0.001 vs. PBS) and astrocytes (CC; p=0.003 vs. PBS, ON; p=0.04 vs. PBS) both in CC and ON. There were no alterations in cathepsin B activity in these regions. Conclusions The present study indicates that CSTC could suppress chronic ischemia-induced WMLs and the inhibition of proteases other than cathepsin B may be implicated in this beneficial effect.
    Type of Medium: Online Resource
    ISSN: 0039-2499 , 1524-4628
    URL: Article
    DOI: 10.1161/str.43.suppl_1.A2513
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2012
    detail.hit.zdb_id: 1467823-8
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