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The effect of hydrodynamic-based delivery of an interleukin-13-Ig fusion gene for experimental autoimmune myocarditis in rats and its possible mechanism
http://hdl.handle.net/10191/1159
http://hdl.handle.net/10191/1159a70f3548-4c5f-4138-94d2-584c3ed2b69a
名前 / ファイル | ライセンス | アクション |
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22_0003.pdf (605.1 kB)
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Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2007-04-23 | |||||
タイトル | ||||||
言語 | en | |||||
タイトル | The effect of hydrodynamic-based delivery of an interleukin-13-Ig fusion gene for experimental autoimmune myocarditis in rats and its possible mechanism | |||||
言語 | ||||||
言語 | eng | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | myocarditis | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | autoimmune | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | dilated cardiomyopathy | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | immune system | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | interleukin-13 | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | gene therapy | |||||
資源タイプ | ||||||
資源 | http://purl.org/coar/resource_type/c_6501 | |||||
タイプ | journal article | |||||
著者 |
Elnaggar, Raafat
× Elnaggar, Raafat× Hanawa, Haruo× Liu, Hui× Yoshida, Tsuyoshi× Hayashi, Manabu× Watanabe, Ritsuo× Abe, Satoru× Toba, Ken× Yoshida, Kaori× Chang, He× Minagawa, Shiro× Okura, Yuji× Kato, Kiminori× Kodama, Makoto× Maruyama, Hiroki× Miyazaki, Junichi× Aizawa, Yoshifusa |
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著者別名 | ||||||
識別子 | 4786 | |||||
識別子Scheme | WEKO | |||||
姓名 | 塙, 晴雄 | |||||
抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Interleukin (IL)-13 is a pleiotropic cytokine secreted by activated Th2-T lymphocytes. Th1 cytokines are assumed to exacerbate while Th2 cytokines to ameliorate rat experimental autoimmune myocarditis (EAM). Here, we examined the effect of IL-13 on EAM using a hydrodynamic-based delivery of an IL-13-Ig and the possible mechanism of its effect. Rats were immunized on day 0 and IL-13-Ig treated rats were injected with pCAGGS-IL-13-Ig and control rats with pCAGGS-Ig on day 1 or 7. On day 17, IL-13-Ig gene therapy was effective in controlling EAM as monitored by the decreased heart weight/body weight ratio, reduced myocarditis and atrial natriuretic peptide mRNA in heart as a heart failure marker. On the basis of IL-13 receptor mRNA expression in separated cells from EAM hearts, we proposed that IL-13-Ig targeting cells were CD11b+ cells and non-cardiomyocytic non-inflammatory (NCNI) cells such as fibroblasts, smooth muscle or endothelial cells. IL-13-Ig inhibited expressing the genes of prostaglandin E synthase, cyclooxygenase-2, inducible nitric oxide synthase, IL-1β and TNFα of cultivated cells from EAM hearts in contrast, while it enhanced IL-1 receptor antagonist. We concluded that IL-13-Ig ameliorates EAM and supposed that its effectiveness may be due to the influence on these immunologic molecules in CD11b+ and NCNI cells. | |||||
書誌情報 |
European journal of immunology en : European journal of immunology 巻 35, 号 6, p. 1995-2005, 発行日 2005-06 |
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ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 00142980 | |||||
書誌レコードID | ||||||
収録物識別子タイプ | NCID | |||||
収録物識別子 | AA00639610 | |||||
PubMed番号 | ||||||
識別子タイプ | PMID | |||||
関連識別子 | 15902684 | |||||
DOI | ||||||
識別子タイプ | DOI | |||||
関連識別子 | info:doi/10.1002/eji.200425776 | |||||
権利 | ||||||
権利情報 | WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim | |||||
著者版フラグ | ||||||
値 | author |