In vivo transfer of soluble TNF-alpha receptor 1 gene improves cardiac function and reduces infarct size after myocardial infarction in rats 1 MASAHIRO SUGANO 2 , KEIKO TSUCHIDA, TOMOJI HATA and NAOKI MAKINO Department of Molecular and Cellular Biology, Division of Molecular and Clinical Gerontology, Medical Institute of Bioregulation, Kyushu University, Beppu, Japan 2 Correspondence: Department of Molecular and Cellular Biology, Division of Molecular and Clinical Gerontology, Medical Institute of Bioregulation, Kyushu University, 4546 Tsurumihara, Beppu, Oita, 874-0838, Japan. Email: massy@tsurumi.beppu.kyushu-u.ac.jp <h3>SPECIFIC AIMS</h3> Soluble TNF-α receptor 1 (sTNFR1) is an extracellular domain of TNFR1 and an antagonist to TNF-α. Recently, we demonstrated that transfection of sTNFR1 expression plasmid DNA to the heart reduced TNF-α bioactivity in the heart and thereby protected the myocardium from acute myocardial infarction (AMI) in vivo. We hypothesized that anti-TNF therapy with sTNFR1 might also have effect on cardiac function since TNF-α levels are increased in heart failure. In the present study, we examined effects of sTNFR1 on cardiac function and infarct size after myocardial infarction in rats. <h3>PRINCIPAL FINDINGS</h3> <h3>1. Plasmid construction and soluble TNF receptor 1 expression</h3> Gene encoding a soluble form of rat type 1 TNF receptor (extracellular domain of rat
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In vivo transfer of soluble TNF-alpha receptor 1 gene improves cardiac function and reduces infarct size after myocardial infarction in rats
SUGANO, MASAHIRO; TSUCHIDA, KEIKO; HATA, TOMOJI; MAKINO, NAOKI
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, Volume 18 (7): 911
Fed of American Socs for Experimental Biology – May 1, 2004
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