ジュウジョウ　ケンタロウ   JUJO Kentaro   重城　健太郎    所属   埼玉医科大学  医学部 総合医療センター　心臓内科    職種   教授
論文種別	学術雑誌(原著)
言語種別	英語
査読の有無	査読あり
表題	CXC-Chemokine Receptor 4 Antagonist AMD3100 Promotes Cardiac Functional Recovery After Ischemia/Reperfusion Injury via Endothelial Nitric Oxide Synthase-Dependent Mechanism
掲載誌名	正式名：CIRCULATION ISSNコード：00097322
出版社	LIPPINCOTT WILLIAMS&WILKINS
巻・号・頁	127(1),63-+頁
著者・共著者	Kentaro Jujo,Masaaki Ii,Haruki Sekiguchi,Ekaterina Klyachko,Sol Misener,Toshikazu Tanaka,Joern Tongers,Jerome Roncalli,Marie-Ange Renault,Tina Thorne,Aiko Ito,Trevor Clarke,Christine Kamide,Yukio Tsurumi,Nobuhisa Hagiwara,Gangjian Qin,Michio Asahi,Douglas W. Losordo
発行年月	2013/01
概要	Background-CXC-chemokine receptor 4 (CXCR4) regulates the retention of stem/progenitor cells in the bone marrow (BM), and the CXCR4 antagonist AMD3100 improves recovery from coronary ligation injury by mobilizing stem/progenitor cells from the BM to the peripheral blood. Thus, we investigated whether AMD3100 also improves recovery from ischemia/reperfusion injury, which more closely mimics myocardial infarction in patients, because blood flow is only temporarily obstructed.Methods and Results-Mice were treated with single subcutaneous injections of AMD3100 (5 mg/kg) or saline after ischemia/reperfusion injury. Three days later, histological measurements of the ratio of infarct area to area at risk were smaller in AMD3100-treated mice than in mice administered saline, and echocardiographic measurements of left ventricular function were greater in the AMD3100-treated mice at week 4. CXCR4(+) cells were mobilized for just 1 day in both groups, but the mobilization of sca1(+)/flk1(+) cells endured for 7 days in AMD3100-treated mice compared with just 1 day in the saline-treated mice. AMD3100 upregulated BM levels of endothelial nitric oxide synthase (eNOS) and 2 targets of eNOS signal
DOI	10.1161/CIRCULATIONAHA.112.099242