Long noncoding RNA Alu-mediated p21 transcriptional regulator promotes proliferation, migration, and pipe-formation of human microvascular endothelial cells by sponging miR-126.

Peripheral artery disease (PAD) is a serious hazard to the elderly in the lower extremity atherosclerotic plaque, accompanied by a large number of angiogenesis. Long noncoding RNA Alu-mediated p21 transcriptional regulator (APTR) exerts important functions in promoting cell growth. Therefore, we planned to research the mechanism of APTR in angiogenesis in PAD. CCK-8 assay, flow cytometry analysis, and migration assay were to detect cell viability, apoptosis, and migration respectively. The interaction between APTR and miR-12 was tested through luciferase activity test. In vitro angiogenesis assay was used to test the number of tubular cells. qRT-PCR and Western blot were to test expression of APTR, miR-126, and angiogenesis relative factors. There was spontaneously pipe-formation in HEMC-1 cells under matrigel condition. Knockdown of APTR inhibited cell viability and migration and reduced the number of tubular cells. Further, APTR sponged miR-126 and downregulating miR-126 to promote angiogenesis. Overexpression of APTR promoted cell activity and migration and increased the number of tubular cells via negatively regulating miR-126. APTR could elevate activating phosphatidylinositol 3 kinase/protein kinase B and mitogen extracellular kinase/extracellular signal-regulated kinase signal pathways via negatively regulating miR-126 to promote cell proliferation, migration, and pipe-formation. We researched the mechanism of angiogenesis that APTR elevated proliferation, migration, and pipe-formation via negatively regulating miR-126.