In vivo gene transfer of soluble TNF-alpha receptor 1 alleviates myocardial infarction.

Masahiro Sugano; Masamichi Koyanagi; Keiko Tsuchida; Tomoji Hata; Naoki Makino

doi:10.1096/fj.01-0894fje

In vivo gene transfer of soluble TNF-alpha receptor 1 alleviates myocardial infarction.

Masahiro Sugano, Masamichi Koyanagi, Keiko Tsuchida, Tomoji Hata, Naoki Makino

Research output: Contribution to journal › Article › peer-review

23 Citations (Scopus)

Abstract

Apoptosis is the major independent form of cardiomyocyte cell death in acute myocardial infarction (AMI). TNF-alpha release early in the course of AMI contributes to myocardial injury, and TNF-alpha induces apoptosis in cardiomyocytes. Soluble TNF-alpha receptor 1 (sTNFR1) is an antagonist to TNF-alpha. However, the effect of sTNFR1 on AMI remains unclear. Here we report that direct injection of an sTNFR1 expression plasmid DNA to the myocardium reduces infarct size in experimental rat AMI. Treatment with sTNFR1 expression plasmid DNA reduced the TNF-alpha bioactivity in the myocardium and the apoptosis of cardiomyocytes. These findings suggest that the anti-TNF-alpha therapy by sTNFR1 can be a new strategy for treatment of AMI.

Original language	English
Pages (from-to)	1421-1422
Number of pages	2
Journal	The FASEB journal : official publication of the Federation of American Societies for Experimental Biology
Volume	16
Issue number	11
DOIs	https://doi.org/10.1096/fj.01-0894fje
Publication status	Published - 2002
Externally published	Yes

All Science Journal Classification (ASJC) codes

Biotechnology
Biochemistry
Molecular Biology
Genetics

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Cite this

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title = "In vivo gene transfer of soluble TNF-alpha receptor 1 alleviates myocardial infarction.",

abstract = "Apoptosis is the major independent form of cardiomyocyte cell death in acute myocardial infarction (AMI). TNF-alpha release early in the course of AMI contributes to myocardial injury, and TNF-alpha induces apoptosis in cardiomyocytes. Soluble TNF-alpha receptor 1 (sTNFR1) is an antagonist to TNF-alpha. However, the effect of sTNFR1 on AMI remains unclear. Here we report that direct injection of an sTNFR1 expression plasmid DNA to the myocardium reduces infarct size in experimental rat AMI. Treatment with sTNFR1 expression plasmid DNA reduced the TNF-alpha bioactivity in the myocardium and the apoptosis of cardiomyocytes. These findings suggest that the anti-TNF-alpha therapy by sTNFR1 can be a new strategy for treatment of AMI.",

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T1 - In vivo gene transfer of soluble TNF-alpha receptor 1 alleviates myocardial infarction.

AU - Sugano, Masahiro

AU - Koyanagi, Masamichi

AU - Tsuchida, Keiko

AU - Hata, Tomoji

AU - Makino, Naoki

PY - 2002

Y1 - 2002

N2 - Apoptosis is the major independent form of cardiomyocyte cell death in acute myocardial infarction (AMI). TNF-alpha release early in the course of AMI contributes to myocardial injury, and TNF-alpha induces apoptosis in cardiomyocytes. Soluble TNF-alpha receptor 1 (sTNFR1) is an antagonist to TNF-alpha. However, the effect of sTNFR1 on AMI remains unclear. Here we report that direct injection of an sTNFR1 expression plasmid DNA to the myocardium reduces infarct size in experimental rat AMI. Treatment with sTNFR1 expression plasmid DNA reduced the TNF-alpha bioactivity in the myocardium and the apoptosis of cardiomyocytes. These findings suggest that the anti-TNF-alpha therapy by sTNFR1 can be a new strategy for treatment of AMI.

AB - Apoptosis is the major independent form of cardiomyocyte cell death in acute myocardial infarction (AMI). TNF-alpha release early in the course of AMI contributes to myocardial injury, and TNF-alpha induces apoptosis in cardiomyocytes. Soluble TNF-alpha receptor 1 (sTNFR1) is an antagonist to TNF-alpha. However, the effect of sTNFR1 on AMI remains unclear. Here we report that direct injection of an sTNFR1 expression plasmid DNA to the myocardium reduces infarct size in experimental rat AMI. Treatment with sTNFR1 expression plasmid DNA reduced the TNF-alpha bioactivity in the myocardium and the apoptosis of cardiomyocytes. These findings suggest that the anti-TNF-alpha therapy by sTNFR1 can be a new strategy for treatment of AMI.

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In vivo gene transfer of soluble TNF-alpha receptor 1 alleviates myocardial infarction.

Abstract

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