TNFR gene-modified mesenchymal stem cells attenuate inflammation and cardiac dysfunction following MI

Scand Cardiovasc J. 2008 Feb;42(1):56-62. doi: 10.1080/14017430701543556.

Abstract

Objectives: To investigate the protective effect of tumor necrosis factor receptor (TNFR) gene modified mesenchymal stem cells (MSCs) transplantation against inflammation and cardiac dysfunction following acute myocardial infarction (AMI).

Design: MSCs were extracted from the tibias and femurs of rats and transfected with recombinant adeno-associated viral (rAAV) expressing EGFP (enhanced green fluorescent protein) or p75 (human 75 kilodalton) TNFR at multiplicity of infection of 10(5) particles/cell. Rats with AMI induced by occlusion of the left coronary artery were randomized to MSCs-TNFR transplantation group, MSCs-EGFP transplantation group and MI control group.

Results: The effects of MSCs-TNFR transplantation on cardiac inflammation and left ventricular dysfunction were observed after 2 weeks of MI. We found that: 1) MSCs-TNFR transplantation attenuated protein production and gene expression of inflammatory cytokines TNF-, IL-1beta and IL-6; 2) MSCs-TNFR transplantation inhibited cardiomyocytes apoptosis and 3) MSCs-TNFR transplantation improved left ventricular function.

Conclusions: The experimental data show that transplantation with rAAV-TNFR transfected MSCs improves left ventricular function following MI through anti-apoptotic and anti-inflammatory mechanisms.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis
  • Cells, Cultured
  • Dependovirus / genetics
  • Disease Models, Animal
  • Down-Regulation
  • Genetic Therapy / methods*
  • Genetic Vectors
  • Humans
  • Inflammation Mediators / metabolism
  • Interleukin-1beta / metabolism
  • Interleukin-6 / metabolism
  • Male
  • Mesenchymal Stem Cell Transplantation*
  • Mesenchymal Stem Cells / metabolism*
  • Myocardial Infarction / complications
  • Myocardial Infarction / genetics
  • Myocardial Infarction / metabolism
  • Myocardial Infarction / surgery
  • Myocardial Infarction / therapy*
  • Myocarditis / etiology
  • Myocarditis / genetics
  • Myocarditis / metabolism
  • Myocarditis / prevention & control*
  • Myocytes, Cardiac / metabolism*
  • Myocytes, Cardiac / pathology
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, Tumor Necrosis Factor, Type II / genetics
  • Receptors, Tumor Necrosis Factor, Type II / metabolism*
  • Time Factors
  • Transfection
  • Tumor Necrosis Factor-alpha / metabolism
  • Ventricular Dysfunction, Left / etiology
  • Ventricular Dysfunction, Left / genetics
  • Ventricular Dysfunction, Left / metabolism
  • Ventricular Dysfunction, Left / prevention & control*

Substances

  • Inflammation Mediators
  • Interleukin-1beta
  • Interleukin-6
  • Receptors, Tumor Necrosis Factor, Type II
  • TNFRSF1B protein, human
  • Tumor Necrosis Factor-alpha