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 6. LncRNA MALAT1 directly targets miR-15b-5p to promote CAD progression. (A) The predicted binding site. (B) Luciferase activity was declined notably when HEK 293T cells were co-transfected with MALAT1 wild type and miR-15b-5p mimics. **P<0.01, compared with NC group. (C) Expression of miR-15b-5p was increased in both miR-15b-5p mimics and sh-MALAT1#1 groups whereas down-regulated in miR-15b-5p inhibitor group. MiR-15b-5p inhibitor + sh-MALAT1#1 group and miR-15b-5p mimics + pCMV6-MALAT1 were consistent with NC group. **P<0.01, compared with NC group. (D) MTT results illustrated that miR-15b-5p mimics and CCCP strengthened cell viability of EPCs and miR-15b-5p inhibitor suppressed cell viability of EPCs. Co-transfection of miR-15b-5p inhibitor and sh-MALAT1#1 / miR-15b-5p mimics and pCMV6-MALAT1 led to similar results of the NC group. *P<0.05, **P<0.01, compared with NC group. (E) FCM results revealed that both miR-15b-5p mimics and CCCP repressed cell apoptosis rate of EPCs while miR-15b-5p inhibitor promoted apoptosis rate. Co-transfection of miR-15b-5p inhibitor and sh-MALAT1#1 / miR-15b-5p mimics and pCMV6-MALAT1 had little influence on cell apoptosis rate of EPCs. **P<0.01, compared with NC group. (F) Autophagy assay revealed that both miR-15b-5p mimics and CCCP promoted EPCs autophagy while miR-15b-5p inhibitor repressed cell autophagy. Co-transfection of miR-15b-5p inhibitor and sh-MALAT1#1 / miR-15b-5p mimics and pCMV6-MALAT1 had little influence on cell autophagy. **P<0.01, compared with NC group.