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In vivo gene transfer of soluble TNF‐α receptor 1 alleviates myocardial infarction
Author(s) -
Sugano Masahiro,
Koyanagi Masamichi,
Tsuchida Keiko,
Hata Tomoji,
Makino Naoki
Publication year - 2002
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.01-0894fje
Subject(s) - apoptosis , tumor necrosis factor alpha , in vivo , myocardial infarction , receptor , medicine , alpha (finance) , genetic enhancement , antagonist , pharmacology , cancer research , endocrinology , gene , chemistry , biology , surgery , biochemistry , genetics , construct validity , patient satisfaction
ABSTRACT Apoptosis is the major independent form of cardiomyocyte cell death in acute myocardial infarction (AMI). TNF‐α release early in the course of AMI contributes to myocardial injury, and TNF‐α induces apoptosis in cardiomyocytes. Soluble TNF‐alpha receptor 1 (sTNFR1) is an antagonist to TNF‐α. 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‐α bioactivity in the myocardium and the apoptosis of cardiomyocytes. These findings suggest that the anti‐TNF‐α therapy by sTNFR1 can be a new strategy for treatment of AMI.