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KAKEN_17K15625seika.pdf
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Download
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:150.7 KB
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:Oct 31, 2019 |
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Total downloads since Oct 31, 2019 : 152
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4回膜貫通タンパク質Tspan18を介した血管形成機能の解明
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4カイ マク カンツウ タンパクシツ Tspan18 オ カイシタ ケッカン ケイセイ キノウ ノ カイメイ
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4kai maku kantsū tanpakushitsu Tspan18 o kaishita kekkan keisei kinō no kaimei
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Mechanistic elucidation of angiogenesis mediated by Tspan18
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田井, 育江
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タイ, イクエ
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Tai, Ikue
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慶應義塾大学・医学部 (信濃町)・講師
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Research team head
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科研費研究者番号 : 90749508
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2019
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科学研究費補助金研究成果報告書
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2018
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4回膜貫通タンパク質Tspan18を血管内皮細胞において欠損するマウスが血管発生に異常を示す機構を明らかにするため、Tspan18とVEGF受容体との結合を評価し、酵素的切断により生じるVEGFR2の130kDaおよび75kDaの断片がTspan18と結合することを明らかにした。また、130kDa断片の産生はメタロプロテアーゼ阻害剤により阻害されること、および、Tspan18をノックダウンした血管内皮細胞では2つの断片のターンオーバーが変化することを見出した。Tspan18欠損マウスに腫瘍を移植して形成される腫瘍血管は、正常血管に近い性質を示し、腫瘍血管で通常見られる出血が見られなかった。
Tspan18-dificient mice show abnormality in retinal vascular development. To understand how this phenotype is induced, binding of Tspan18 to VEGFRs was evaluated by co-immunoprecipitation assay. As a result, binding of Tspan18 to proteolytic fragments of VEGFR2, 130-kDa and 75-kDa fragments, was detected. Experiments using protease inhibitors showed that metalloprotease is necessary for the production of the 130-kDa fragment. Furthermore, it was shown that knockdown of Tspan18 in blood endothelial cells results in a shift in turnover of the fragments, including enhanced production of 130-kDa fragment and delayed production of 75-kDa fragment after VEGF treatment. Tumor blood vessels in Tspan18-deficient mice showed normalization of vascular structure, including absence of hemorrhage.
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研究種目 : 若手研究(B)
研究期間 : 2017～2018
課題番号 : 17K15625
研究分野 : 血管生物学
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