Research Paper Volume 13, Issue 8 pp 11135—11149

WTAP promotes myocardial ischemia/reperfusion injury by increasing endoplasmic reticulum stress via regulating m6A modification of ATF4 mRNA

WTAP knockdown inhibits I/R injury in vivo. WTAP shRNA or negative control (shNC) was injected into rats. (A, B) H&E and TUNEL staining analysis of myocardium of rats. Scale bar: 50 μm. (C) The m6A levels in myocardium of rats were measured by ELISA. (D, E) Expression levels of WTAP, cleaved PARP, cleaved Caspase-3, ATF4 and CHOP in myocardial cells of rats. (F) Schematic diagram of the relationships among WTAP, m6A modification, and cell apoptosis under I/R condition. All experiments were repeated at least three times, and data are represented as mean ± SD. ***P ###P

Figure 6. WTAP knockdown inhibits I/R injury in vivo. WTAP shRNA or negative control (shNC) was injected into rats. (A, B) H&E and TUNEL staining analysis of myocardium of rats. Scale bar: 50 μm. (C) The m6A levels in myocardium of rats were measured by ELISA. (D, E) Expression levels of WTAP, cleaved PARP, cleaved Caspase-3, ATF4 and CHOP in myocardial cells of rats. (F) Schematic diagram of the relationships among WTAP, m6A modification, and cell apoptosis under I/R condition. All experiments were repeated at least three times, and data are represented as mean ± SD. ***P < 0.0001 vs control (without LAD ligation). ###P < 0.001 vs I/R+shNC.