Cytokine gene therapy for myocarditis by in vivo electroporation

Hum Gene Ther. 2001 Jul 1;12(10):1289-97. doi: 10.1089/104303401750270940.

Abstract

Cytokines are important pathophysiologic and pathogenic factors in cardiovascular disorders, including viral myocarditis. We attempted to treat viral myocarditis with cytokine gene therapy by transferring an inhibitory cytokine, IL-1 receptor antagonist (IL-1ra) or viral IL-10 (vIL-10), by in vivo electroporation, a new method for gene transfer into muscle. Four-week-old male DBA/2 mice were inoculated intraperitoneally with 10 PFU of encephalomyocarditis virus. Immediately after virus inoculation, an expression plasmid carrying IL-1ra or vIL-10 was injected into tibialis anterior muscles followed by electroporation. Serum levels of IL1ra and vIL-10 reached 10.5 and 2.3 ng/ml, respectively, on day 5, when gene expression reached its peak. Histopathological examination showed that myocardial cellular infiltration was improved in mice treated with IL-1ra or vIL-10 compared with the control group. On day 14 after the onset of myocarditis, transfer of IL1ra or vIL-10 expression plasmid had significantly improved the survival rates of the animals. The expression of TNF-alpha was decreased to 0.60-fold (p < 0.005) and inducible nitric oxide synthase (iNOS) 0.43-fold (p < 0.005) by IL-1ra treatment, and the expression of IFN-gamma in the heart was decreased to 0.35-fold (p < 0.05), and iNOS 0.21-fold (p < 0.005), by vIL-10 relative to the controls. These results show that gene therapy with IL-1ra or vIL-10 expression plasmid was effective in the treatment of viral myocarditis, and in vivo electroporation may be a useful method by which to deliver cytokine therapy in cardiovascular diseases.

MeSH terms

  • Animals
  • Blotting, Western
  • Cytokines / genetics*
  • DNA, Complementary / metabolism
  • Electrophoresis, Polyacrylamide Gel
  • Electroporation / methods*
  • Encephalomyocarditis virus / genetics
  • Enzyme-Linked Immunosorbent Assay
  • Gene Transfer Techniques*
  • Genetic Therapy / methods*
  • Genetic Vectors
  • Interleukin-10 / blood
  • Interleukin-10 / genetics
  • Male
  • Mice
  • Mice, Inbred DBA
  • Muscles / metabolism
  • Myocarditis / therapy*
  • Myocardium / metabolism
  • Nitric Oxide Synthase / biosynthesis
  • Nitric Oxide Synthase Type II
  • Plasmids / genetics
  • Plasmids / metabolism
  • Rats
  • Receptors, Interleukin-1 / antagonists & inhibitors
  • Receptors, Interleukin-1 / genetics
  • Reverse Transcriptase Polymerase Chain Reaction
  • Time Factors
  • Tumor Necrosis Factor-alpha / biosynthesis

Substances

  • Cytokines
  • DNA, Complementary
  • Receptors, Interleukin-1
  • Tumor Necrosis Factor-alpha
  • Interleukin-10
  • Nitric Oxide Synthase
  • Nitric Oxide Synthase Type II
  • Nos2 protein, mouse
  • Nos2 protein, rat