Research Paper Volume 11, Issue 4 pp 1089—1109

MALAT1/miR-15b-5p/MAPK1 mediates endothelial progenitor cells autophagy and affects coronary atherosclerotic heart disease via mTOR signaling pathway

Figure 7. MAPK1 as a functional target of miR-15b-5p regulates CAD progression. (A) The predicted binding site. (B) Co-transfection of MAPK1 wild type and miR-15b-5p mimics decreased luciferase activity. **P<0.01, compared with NC group. (C) MAPK1 was down-regulated by CCCP while up-regulated by pCMV6-MAPK1. MiR-15b-5p mimics + pCMV6-MAPK1 group was aligned with NC group. **P<0.01, compared with NC group. (D) MTT results demonstrated that cell viability of EPCs were promoted by CCCP and inhibited by pCMV6-MAPK1. MiR-15b-5p mimics + pCMV6-MAPK1 group had almost no influence on cell viability of EPCs. **P<0.01, compared with NC group. (E) FCM results illustrated that CCCP group presented declined apoptosis rate of EPCs while pCMV6-MAPK1 group presented increased apoptosis rate. MiR-15b-5p mimics + pCMV6-MAPK1 group presented the same apoptosis rate as NC group. **P<0.01, compared with NC group. (F) Autophagy results illustrated that CCCP group accelerated EPCs autophagy while pCMV6-MAPK1 group presented declined autophagy. MiR-15b-5p mimics + pCMV6-MAPK1 group presented the same autophagy as NC group. **P<0.01, compared with NC group.