Effect and functional mechanism of induced pluripotent stem cells on myocardial fibrosis after cardiac infarction

Acute myocardial infarction (AMI) has a high incidence and causes severe consequences. Induced plu- ripotent stem (iPS) cells derives from patient’s own cells and has become one research focus for treating cardiovas- cular disease. The role and function of iPS cells on myocardial fibrosis after AMI, however, has not been illustrated. Healthy male Wistar rats were randomly divided into control, sham and AMI group. The AMI model was generated by occlusion of left anterior coronary artery. iPS cell transplantation group received mouse derived iPS cells after AMI model. M-type ultrasound was used to evaluate cardiac function of all rats. Immunohistochemistry staining was employed to evaluate the change of myocardial fibrosis. ELISA was adopted for measuring type I collagen content. Real time PCR and Western blotting were employed to quantify mRNA and protein levels of Bax or Bcl-2 in myocar- dial tissues, respectively. Left ventricular end-stage systolic dimeter (LVEDS), leaf ventricular end-stage diabolic di- ameter (LVEDD) and left ventricular mass index (LVMI) were all significantly increased in AMI model rats, which also showed elevated myocardial fibrosis, type I collagen content and Bax expression, along with decreased Bcl-2 mRNA or protein level (P<0.05 compared to sham group). iPS cell transplantation led to lower LVESD, LVEED and LVMI levels accompanied with fewer myocardial fibrosis, type I collage, Bax expression plus increased Bcl-2 expression (P<0.05 compared to AMI group). iPS cells can improve the condition of cardiac infarction and fibrosis via modulat- ing apoptosis balance, protecting myocardial cells and suppressing type I collagen proliferation.