Search results for: Sangmee Ahn Jo

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Jo</title> <meta name="description" content="Search results for: Sangmee Ahn Jo"> <meta name="keywords" content="Sangmee Ahn Jo"> <meta name="viewport" content="width=device-width, initial-scale=1, minimum-scale=1, maximum-scale=1, user-scalable=no"> <meta charset="utf-8"> <link href="https://cdn.waset.org/favicon.ico" type="image/x-icon" rel="shortcut icon"> <link href="https://cdn.waset.org/static/plugins/bootstrap-4.2.1/css/bootstrap.min.css" rel="stylesheet"> <link href="https://cdn.waset.org/static/plugins/fontawesome/css/all.min.css" rel="stylesheet"> <link href="https://cdn.waset.org/static/css/site.css?v=150220211555" rel="stylesheet"> </head> <body> <header> <div class="container"> <nav class="navbar navbar-expand-lg navbar-light"> <a class="navbar-brand" href="https://waset.org"> <img src="https://cdn.waset.org/static/images/wasetc.png" alt="Open Science Research Excellence" title="Open Science Research Excellence" /> </a> <button class="d-block d-lg-none navbar-toggler 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id="custom-search-input"> <div class="input-group"> <i class="fas fa-search"></i> <input type="text" class="search-query" name="q" placeholder="Author, Title, Abstract, Keywords" value="Sangmee Ahn Jo"> <input type="submit" class="btn_search" value="Search"> </div> </div> </form> </div> </div> <div class="row mt-3"> <div class="col-sm-3"> <div class="card"> <div class="card-body"><strong>Commenced</strong> in January 2007</div> </div> </div> <div class="col-sm-3"> <div class="card"> <div class="card-body"><strong>Frequency:</strong> Monthly</div> </div> </div> <div class="col-sm-3"> <div class="card"> <div class="card-body"><strong>Edition:</strong> International</div> </div> </div> <div class="col-sm-3"> <div class="card"> <div class="card-body"><strong>Paper Count:</strong> 3</div> </div> </div> </div> <h1 class="mt-3 mb-3 text-center" style="font-size:1.6rem;">Search results for: Sangmee Ahn Jo</h1> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">3</span> Depressant Effects of 2-PMPA through Reduction of p-CREB (Ser133) and mGluR5 Level in Prefrontal Cortex of C57BL/6 Mice</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Sang-Sun%20Yoon">Sang-Sun Yoon</a>, <a href="https://publications.waset.org/abstracts/search?q=Yea-Hyun%20Leem"> Yea-Hyun Leem</a>, <a href="https://publications.waset.org/abstracts/search?q=Sangmee%20Ahn%20Jo"> Sangmee Ahn Jo</a> </p> <p class="card-text"><strong>Abstract:</strong></p> The N-acetylated-alpha-linked-acidic (NAAG) peptidase inhibitor 2-phosphonomethyl pentanedioic acid (2-PMPA) has demonstrated to be neuroprotective against glutamate-mediated neuron degeneration and neurological disorders such as ischemia. Several studies have demonstrated impaired psychiatric function by altered glutamate carboxypeptidase II expression, although 2-PMPA has not yet been studied. Thus, we investigated effect of 2-PMPA on depressive-like phenotype using C57BL/6 mice. Treatment of 2-PMPA (10 mg/kg for 6 days/daily, ip injection) on C57BL/6 na茂ve mice showed depressive-like symptoms such as decreased social preference, but did not affect the immobility measured by tail suspension test. Reduction of phosphorylated cAMP-responsive element binding (p-CREB) known as a representative marker of depressive-like behavior was observed in layer 1 and piriform cortex subregions of the prefrontal cortex of 2-PMPA-treated mice. The immunoreactivity of metabotropic glutamate receptors 5 (mGluR5) that mediate phosphorylation of CREB was also decreased in layer 1 and piriform cortex subregions of the prefrontal cortex of 2-PMPA injected mice. Thus, our results suggest that dysregulation of the GCPII or NAAG by 2-PMPA treatment is likely to be associated with pathogenesis of depression and further studies are needed to understand whether the reduced NAAG level or enhanced glutamate level in the brain is involved in this response. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=depression" title="depression">depression</a>, <a href="https://publications.waset.org/abstracts/search?q=GCPII" title=" GCPII"> GCPII</a>, <a href="https://publications.waset.org/abstracts/search?q=2-PMPA" title=" 2-PMPA"> 2-PMPA</a>, <a href="https://publications.waset.org/abstracts/search?q=p-CREB" title=" p-CREB"> p-CREB</a>, <a href="https://publications.waset.org/abstracts/search?q=mGluR5" title=" mGluR5"> mGluR5</a> </p> <a href="https://publications.waset.org/abstracts/39642/depressant-effects-of-2-pmpa-through-reduction-of-p-creb-ser133-and-mglur5-level-in-prefrontal-cortex-of-c57bl6-mice" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/39642.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">266</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">2</span> ICAM1 Expression is Enhanced by TNFa through Histone Methylation in Human Brain Microvessel Cells</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Ji-Young%20Choi">Ji-Young Choi</a>, <a href="https://publications.waset.org/abstracts/search?q=Jungjin%20Kim"> Jungjin Kim</a>, <a href="https://publications.waset.org/abstracts/search?q=Sang-Sun%20Yun"> Sang-Sun Yun</a>, <a href="https://publications.waset.org/abstracts/search?q=Sangmee%20Ahn%20Jo"> Sangmee Ahn Jo</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Intracellular adhesion molecule1 (ICAM1) is a mediator of inflammation and involved in adhesion and transmigration of leukocytes to endothelial cells, resulting in enhancement of brain inflammation. We hypothesized that increase of ICAM1 expression in endothelial cells is an early step in the pathogenesis of brain diseases such as Alzheimer鈥檚 disease. Here, we report that ICAM1 expression is regulated by pro-inflammatory cytokine TNFa in human microvascular endothelial cell (HBMVEC). TNFa significantly increased ICAM1 mRNA and protein levels at the concentrations showing no cell toxicity. This increase was also shown in micro vessels of mouse brain 24 hours after treatment with TNFa (8 mg/kg, i.v). We then investigated the epigenetic mechanism involved in the induction of ICAM1 expression. Chromatin immunoprecipitation assay revealed that TNFa reduced methylation of histone3K9 (H3K9-2me) and histone3K27 (H3K27-3me), well-known modification as gene suppression, with in the ICAM1 promoter region. However, acetylation of H3K9 and H3K14, well-known modification as gene activation, was not changed by TNFa. Treatment of BIX01294, a specific inhibitor of histone methyltransferase G9a responsible for H3K9-2me, dramatically increased in ICAM1 mRNA and protein levels and overexpression of G9a gene suppressed TNFa-induced ICAM1 expression. In contrast, GSK126, an inhibitor of histone methyltransferase EZH2 responsible for H3K27-3me and valproic acid, an inhibitor of histone deacetylase (HDAC) did not affect ICAM1 expression. These results suggested that histone3 methylation is involved in ICAM1 repression. Moreover, TNFa or BIX01294-induced ICAM induction resulted in both enhancements in adhesion and transmigration of leukocyte on endothelial cell. This study demonstrates that TNFa upregulates ICAM1 expression through H3K9-2me and H3K27-3me within the ICAM1 promoter region, in which G9a is likely to play a pivotal role in ICAM1 transcription. Our study provides a novel mechanism for ICAM1 transcription regulation in HBMVEC. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=ICAM1" title="ICAM1">ICAM1</a>, <a href="https://publications.waset.org/abstracts/search?q=TNFa" title=" TNFa"> TNFa</a>, <a href="https://publications.waset.org/abstracts/search?q=HBMVEC" title=" HBMVEC"> HBMVEC</a>, <a href="https://publications.waset.org/abstracts/search?q=H3K9-2me" title=" H3K9-2me"> H3K9-2me</a> </p> <a href="https://publications.waset.org/abstracts/39574/icam1-expression-is-enhanced-by-tnfa-through-histone-methylation-in-human-brain-microvessel-cells" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/39574.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">329</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">1</span> Inhibition of Glutamate Carboxypeptidase Activity Protects Retinal Ganglionic Cell Death Induced by Ischemia-Reperfusion by Reducing the Astroglial Activation in Rat</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Dugeree%20Otgongerel">Dugeree Otgongerel</a>, <a href="https://publications.waset.org/abstracts/search?q=Kyong%20Jin%20Cho"> Kyong Jin Cho</a>, <a href="https://publications.waset.org/abstracts/search?q=Yu-Han%20Kim"> Yu-Han Kim</a>, <a href="https://publications.waset.org/abstracts/search?q=Sangmee%20Ahn%20Jo"> Sangmee Ahn Jo</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Excessive activation of glutamate receptor is thought to be involved in retinal ganglion cell (RGC) death after ischemia- reperfusion damage. Glutamate carboxypeptidase II (GCPII) is an enzyme responsible for the synthesis of glutamate. Several studies showed that inhibition of GCPII prevents or reduces cellular damage in brain diseases. Thus, in this study, we examined the expression of GCPII in rat retina and the role of GCPII in acute high IOP ischemia-reperfusion damage of eye by using a GCPII inhibitor, 2-(phosphonomethyl) pentanedioic acid (2-PMPA). Animal model of ischemia-reperfusion was induced by raising the intraocular pressure for 60 min and followed by reperfusion for 3 days. Rats were randomly divided into four groups: either intra-vitreous injection of 2-PMPA (11 or 110 ng per eye) or PBS after ischemia-reperfusion, 2-PMPA treatment without ischemia-reperfusion and sham-operated normal control. GCPII immunoreactivity in normal rat retina was detected weakly in retinal nerve fiber layer (RNFL) and retinal ganglionic cell layer (RGL) and also inner plexiform layer (IPL) and outer plexiform layer (OPL) strongly where are co-stained with an anti-GFAP antibody, suggesting that GCPII is expressed mostly in Muller and astrocytes. Immunostaining with anti-BRN antibody showed that ischemia- reperfusion caused RGC death (31.5 %) and decreased retinal thickness in all layers of damaged retina, but the treatment of 2-PMPA twice at 0 and 48 hour after reperfusion blocked these retinal damages. GCPII level in RNFL layer was enhanced after ischemia-reperfusion but was blocked by PMPA treatment. This result was confirmed by western blot analysis showing that the level of GCPII protein after ischemia- reperfusion increased by 2.2- fold compared to control, but this increase was blocked almost completely by 110 ng PMPA treatment. Interestingly, GFAP immunoreactivity in the retina after ischemia- reperfusion followed by treatment with PMPA showed similar pattern to GCPII, increase after ischemia-reperfusion but reduction to the normal level by PMPA treatment. Our data demonstrate that increase of GCPII protein level after ischemia-reperfusion injury is likely to cause glial activation and/or retinal cell death which are mediated by glutamate, and GCPII inhibitors may be useful in treatment of retinal disorders in which glutamate excitotoxicity is pathogenic. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=glutamate%20carboxypepptidase%20II" title="glutamate carboxypepptidase II">glutamate carboxypepptidase II</a>, <a href="https://publications.waset.org/abstracts/search?q=glutamate%20excitotoxicity" title=" glutamate excitotoxicity"> glutamate excitotoxicity</a>, <a href="https://publications.waset.org/abstracts/search?q=ischemia-reperfusion" title=" ischemia-reperfusion"> ischemia-reperfusion</a>, <a href="https://publications.waset.org/abstracts/search?q=retinal%20ganglion%20cell" title=" retinal ganglion cell"> retinal ganglion cell</a> </p> <a href="https://publications.waset.org/abstracts/39644/inhibition-of-glutamate-carboxypeptidase-activity-protects-retinal-ganglionic-cell-death-induced-by-ischemia-reperfusion-by-reducing-the-astroglial-activation-in-rat" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/39644.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">340</span> </span> </div> </div> </div> </main> <footer> <div id="infolinks" class="pt-3 pb-2"> <div class="container"> <div style="background-color:#f5f5f5;" class="p-3"> <div class="row"> <div class="col-md-2"> <ul class="list-unstyled"> About <li><a href="https://waset.org/page/support">About Us</a></li> <li><a href="https://waset.org/page/support#legal-information">Legal</a></li> <li><a target="_blank" rel="nofollow" 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Search results for: Sangmee Ahn Jo