著者

米満 吉和 居石 克夫

出版者

一般社団法人 日本動脈硬化学会

雑誌

動脈硬化 (ISSN:03862682)

巻号頁・発行日

vol.27, no.6, pp.179-187, 2000-04-20 (Released:2011-09-21)

参考文献数

48

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Virus infection as a pathogen in human vascular diseases has been an important and unsolved issue to be studied. According to Koch's postulates, several conditions should be met to define an organism as a pathogen of human disease: especially, 1) to confirm the whole or a part of structure of microorganism including genomic DNA or RNA in the human material, 2) whether infection of microorganism can induce similar disease in mammals. Several bacterias such as Chlamydia pneumoniae or Hericobactor pylori have been studied according to these postulates, however, it has been hazardous for virus research to establish animal model due to species-specificity or tropism. Human cytomegalovirus (HCMV) is one of these candidates, and HCMV DNA has been frequently detected in the both normal and disordered aorta, however, it is sure that presence of viral genome does not always imply its pathogenecity. As important evidences indicating the pathogenesity of HCMV in human vascular diseases, our recent studies demonstrated virus-specific gene transcription in the surgical specimens of “inflammatory” aortic aneurysms but not in any other human aortic tissue, and also exhibited that the immediate early (IE) gene product stimulates vascular smooth muscle proliferation in rabbit carotid arteries. Whereas these findings suggest the pathogenic ability of HCMV in human vascular tree, some issues to be sollved including the reason why HCMV-IE does not induce any inflammatory response in rabbit. Clearly the immune system is varied among the species and this point should be studied very carefully. Overall, although it seems nearly slow, we consider that the studies for virus etiology in human vascular disorders are now getting progression.

著者

米満 吉和 松本 拓也 前原 喜彦

出版者

学研メディカル秀潤社

雑誌

細胞工学 (ISSN:02873796)

巻号頁・発行日

vol.31, no.4, pp.445-450, 2012

著者

古屋 充子 田中 玲子 米満 吉和 木村 定雄

出版者

横浜市立大学

雑誌

基盤研究(C)

巻号頁・発行日

2008

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炎症性背景をもつ発癌モデルとして内膜症と明細胞腺癌とにおける炎症性微小環境変化を解析した.G蛋白質共役受容体CXCR3を解析したところ,3つの変異体がヒト組織で確認された.定性解析の結果,CXCR3Aは内膜症,癌両者で上昇していた.CXCR3-altは癌で特異的に発現し,CXCR3Bは抑制されていた.CXCL11,CXCL4の発現パターンは各々CXCR3-alt,CXCR3Bと相関した.局在解析では,CXCR3-altは腫瘍血管に,CXCR3Bは正常血管や内膜症血管にシグナルが認められた.以上の結果,G蛋白質共役受容体CXCR3は変異体により発現組織・細胞が異なり,そのリガンド環境も疾患によって異なることが示唆された.CXCR3Bでは抑制性,CXCR3-altでは亢進性シグナルが作動すると予想された.今回期間内では変異体依存性シグナルと4回膜貫通蛋白(TM4)との関連を明らかに出来なかったが,今後は細胞レベルでG蛋白質共役受容体シグナルを介した浸潤・移動能調節機構にインテグリン/TM4がどう応答するか解析する予定である.