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 journalArticle

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 languageEnglish
Pages (from-to)1421-1422
Number of pages2
JournalThe FASEB journal : official publication of the Federation of American Societies for Experimental Biology
Volume16
Issue number11
DOIs
Publication statusPublished - Sep 2002

All Science Journal Classification (ASJC) codes

  • Biotechnology
  • Biochemistry
  • Molecular Biology
  • Genetics

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