Research Paper Volume 12, Issue 4 pp 3156—3174

LncRNA MEG3 targeting miR-424-5p via MAPK signaling pathway mediates neuronal apoptosis in ischemic stroke

Figure 4. The MEG3/miR-424-5p/Sema3A axis affected cell viability and apoptosis in OGD cells via the MAPK pathway. (A) OGD/R cells have lower cell viability compared with control group. Among OGD/R cells, MEG3 downregulation led to higher cell viability, which could be offset by a simultaneous overexpression of Sema3A; miR-424-5p downregulation by its inhibitor led to a lower cell viability compared among OGD/R cells, which could be neutralized by a simultaneous downregulation of Sema3A. *P<0.05 vs control, #P<0.05 vs OGD/R NC, $P<0.05 vs si-MEG3, &P<0.05 vs inhibitor (B, C) OGD/R cells tend to have fairly high apoptosis rate compared to control group. Among OGD/R cells, MEG3 downregulation led to lower cell apoptosis level, which could be neutralized by a simultaneous overexpression of Sema3A; miR-424-5p downregulation by its inhibitor mediated more cell apoptosis, which could be neutralized by a simultaneous downregulation of Sema3A. *P<0.05 vs control, #P<0.05 vs OGD/R NC, $P<0.05 vs si-MEG3, &P<0.05 vs inhibitor. (D) OGD/R cells tend to have higher cleaved caspase-3, p-JNK and p-p38 expression in comparison with control. Among OGD/R cells, the low expression of MEG3 led to a rise in expression of cleaved caspase-3, p-JNK and p-p38, miR-424-5p inhibitor led to drop of expression of cleaved caspase-3, p-JNK and p-p38. Sema3A overexpression could reverse the rise of si-MEG3, while si-Sema3A could reverse the drop of miR-424-5p inhibitor. *P<0.05 vs control, #P<0.05 vs OGD/R NC, $P<0.05 vs si-MEG3, &P<0.05 vs inhibitor.