JaLCDOI 10.18926/AMO/53999
フルテキストURL 70_1_13.pdf
著者 Arum Tri Wahyuningsih| Shen, Lianhua| Kobayashi, Kazuko| Sasaki, Takanori| Takenaka, Fumiaki| Hanada, Takahisa| Akehi, Masaru| Akahoshi, Akiya| Ozeki, Eiichi| Ando, Eiji| Matsuura, Eiji|
抄録 Intact β2-glycoprotein I (iβ2GPI) is a glycoprotein that regulates coagulation and fibrinolysis. Nicked β2GPI (nβ2GPI) possesses an angiogenic property at a relatively low concentration, and an antiangiogenic property at a high concentration. Here we investigated the functions of βi 2GPI and nβ2GPI in vascular endothelial growth factor (VEGF)-A-induced endothelial cell proliferation and tube formation. We used noninvasive PET imaging to analyze the in vivo distribution of intravenously injected β2GPI variants in tumor lesions in mice. iβ2GPI was incubated with plasmin to obtain nβ2GPI, and its N-terminal sequence was analyzed. nβ2GPI had at least one other cleavage site upstream of the β2GPIʼs domain V, whereas the former plasmin-cleavage site locates between K317 and T318. Both of intact and nicked β2GPI significantly inhibited the VEGF-A-induced cell proliferation and the tube formation of human umbilical vein endothelial cells (HUVECs). PET imaging visualized considerably distributed intensities of all tested β2GPI variants in tumor lesions of pancreatic tumor cell-xenografts. These results indicate that β2GPI may be physiologically and pathophysiologically important in the regulation of not only coagulation and fibrinolysis, but also angiogenesis.
キーワード β2-glycoprotein I (β2GPI) angiogenesis vascular endothelial growth factor-A (VEGF-A) positron emission tomography (PET) imaging
Amo Type Original Article
発行日 2016-02
出版物タイトル Acta Medica Okayama
70巻
1号
出版者 Okayama University Medical School
開始ページ 13
終了ページ 24
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 English
著作権者 CopyrightⒸ 2016 by Okayama University Medical School
論文のバージョン publisher
査読 有り
PubMed ID 26899605
Web of Sience KeyUT 000371288700002
著者 松浦 栄次|
発行日 2013-04-01
出版物タイトル 岡山医学会雑誌
125巻
1号
資料タイプ 学術雑誌論文
著者 Matsuura, Eiji| Igarashi, Yoshiko| Yasuda, Tatsuji| Triplett, Douglas A.| Koike, Takao|
発行日 1994-02-01
出版物タイトル Journal of Experimental Medicine
179巻
2号
資料タイプ 学術雑誌論文
JaLCDOI 10.18926/AMO/32848
フルテキストURL fulltext.pdf
著者 Huang, Zhenyu| Liu, Qingping| Li, Wenzhe| Wang, Renjun| Wang, Dan| Zhang, Yingbiao| Zhang, Fan| Chi, Yan| Liu, Zhe| Matsuura, Eiji| Liu, Zibo| Zhang, Qiming|
抄録 <p>We investigated the molecular mechanisms responsible for the induction of apoptosis in mouse monocytic macrophage cell line J774A.1 stimulated by 7-ketocholesterol (7-KC). Cell apoptosis was detected by Annexin V-propidium iodide (PI) staining. The DNA-binding activity of nuclear factor kappa B (NF-kappaB) was assessed by electrophoretic mobility shift assay (EMSA). Results showed that 7-KC-stimulation in J774A.1 cells activated NF-kappaB, which is involved in cell apoptosis, in a time- and dose-dependent manners. 7-KC was also found to increase the binding activity of NF-kappaB to specific DNA binding sites, a possible mechanism for the induction of the cell apoptosis. Moreover, these effects were partially inhibited by pyrrolidine dithiocarbamate (PDTC), an NF-kappaB inhibitor. Taken together, 7-KC may be an important factor in atherosclerosis due to the ability of 7-KC to induce cell apoptosis, which is at least partially mediated through the activation of NF-kappaB.</p>
キーワード 7-KC NF-?B apoptosis atherosclerosis
Amo Type Original Article
発行日 2010-04
出版物タイトル Acta Medica Okayama
64巻
2号
出版者 Okayama University Medical School
開始ページ 85
終了ページ 93
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 English
論文のバージョン publisher
査読 有り
PubMed ID 20424663
Web of Sience KeyUT 000276996900002
著者 松浦 栄次|
発行日 2002-05-30
出版物タイトル 岡山医学会雑誌
114巻
1号
資料タイプ 学術雑誌論文
著者 松浦 栄次|
発行日 1994-03-25
出版物タイトル
資料タイプ 学位論文