The intervention of enalapril maleate and folic acid tablet on the expressions of the GRP78 and CHOP and vascular remodeling in the vascular smooth muscle cells of H-hypertensive rats with homocysteine.

OBJECTIVE: Lower extremity arteriosclerosis is one of leading causes of death worldwide. Arteriosclerosis is closely related to microvascular endothelial cells. This study was aimed to explore the role of long non-coding RNA ROR in regulations of growth, migration, and angiogenesis of microvascular endothelial cells.

MATERIALS AND METHODS: Angiogenesis was determined by the number of tube-like cells on a matrigel extracellular matrix. Cell viability, apoptosis, and migration were determined by CCK-8 assay, PI/FITC-Annexin V staining method, and transwell assay, respectively. Relative RNA expression of ROR, miR-26, and angiogenesis-associated genes were analyzed by qRT-PCR. The protein expression of apoptosis- and angiogenesis-associated genes, as well as main factors in NF-κB and JAK1/STAT3 pathways, were analyzed by Western blot.

RESULTS: LncRNA ROR silence inhibited viability, migration, and angiogenesis of HMEC-1 cells but promoted apoptosis of them. miR-26 expression was promoted after knocking down ROR expression. miR-26 overexpression enhanced the inhibitory effects of ROR silence on growth, migration, and angiogenesis in HMEC-1 cells, whereas, miR-26 silence impaired the effects of ROR silence. Finally, we found that NF-κB and JAK1/STAT3 signaling pathways were inhibited by ROR down-regulation. Similarly, miR-26 overexpression enhanced the inhibitory effect of ROR down-regulation on the pathways and miR-26 inhibition abrogated it.

CONCLUSIONS: Down-regulating lncRNA ROR inhibited growth, migration and angiogenesis of microvascular endothelial cells possibly through up-regulation of miR-26. During this process, the activations of NF-κB and JAK1/STAT3 pathways were inhibited after interaction of ROR and miR-26.