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 4. LncRNA MALAT1 inhibits cell autophagy and promotes CAD progression. (A) MALAT1 and MAPK1 were overexpressed in CAD blood samples and EPCs while miR-15b-5p was down-regulated in CAD blood samples and EPCs. **P<0.01, compared with normal (healthy) group. (B) MALAT1 expression in 5 CAD EPC samples was higher than that in 5 healthy EPC samples. **P<0.01, compared with normal group. (C) MALAT1 was depressed in EPCs transfected with sh-MALAT1#1 or sh-MALAT1#2 detected by qRT-PCR. **P<0.01, compared with NC group. (D) MTT results showed that cell viability was promoted in EPCs transfected with sh-MALAT1#1 or sh-MALAT1#2. **P<0.01, compared with NC group; ##P<0.01, compared with normal group. (E) FCM results revealed that sh-MALAT1#1 or sh-MALAT1#2 restrained cell apoptosis rate of EPCs and there was significant difference between normal group and NC group. *P<0.05, **P<0.01, compared with NC group; ##P<0.01, compared with normal group. (F) Autophagy assay results revealed that sh-MALAT1#1, sh-MALAT1#2 and CCCP raised EPCs autophagy rate and there was conspicuous difference between normal group and NC group. *P<0.05, **P<0.01, compared with NC group; ##P<0.01, compared with normal group.