Research Paper Volume 11, Issue 11 pp 3536—3550

E3-ubiquitin ligase TRIM6 aggravates myocardial ischemia/reperfusion injury via promoting STAT1-dependent cardiomyocyte apoptosis

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Figure 3. TRIM6 promotes myocardial apoptosis after MI/R injury. (AC) The mouse heart was pre-transfected in vivo with control siRNA (siCtrl) or siRNA targeting Trim6 (siTrim6) 48 hrs before surgery. Mice were then subjected to sham surgery or experimental MI/R. Each group contained 7 mice. At 24 hrs after reperfusion, the hearts were harvested for analyses. (A) The myocardial apoptosis in the heart sections was identified by TUNEL staining. The quantitative analysis of TUNEL-positive cardiomyocytes is shown (%). (B) The caspase-3 activity of the heart was measured and expressed as nmol per hr per mg protein. (C) The protein expression of Bax and Bcl-2 was determined by Western blotting analysis. β-Actin was used a loading control. The representative images (left) and the Bax/Bcl-2 ratio relative to sham (right) are shown. (DF) The mouse heart was pre-infected in vivo with lentivirus expressing vector control (LV-vector) or Trim6 (LV-Trim6) 48 hrs before surgery. Mice were then subjected to sham surgery or experimental MI/R. Each group contained 7 mice. At 24 hrs after reperfusion, the hearts were harvested for analyses. The myocardial apoptosis (D), caspase-3 activity (E), and Bax/Bcl-2 ratio (F) in the heart were analyzed as in (AC). All data are expressed as mean ± SD. **, P < 0.01.