Down-regulation of mir-27b promotes angiogenesis and fibroblast activation through activating PI3K/AKT signaling pathway

To study the effects of mir-27b on angiogenesis and fibroblast activation and to explore its further mechanism. Humanmicrovascular endothelial cell (HMEC)-1 and humannormal skin fibroblast (BJ) cells were treated with mir-27b inhibitor negative control reagent, mir-27b inhibitor, LY294002, and mir-27b inhibitor + LY294002, respectively. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) was used to detect the T-cell proliferation. The migration ability was detected by Scratch assays. The angiogenesis of HMEC-1 cells was observed by in vitro tube formation assay. The mRNA and protein expression of vascular endothelial growth factor (VEGF) in HMEC-1 cells and the mRNA and protein expression of collagen I, collagen III, α-SMA, and MMP1 in BJ cells were detected by quantitativereal-time polymerase chain reaction (qRT-PCR) and Western blot, respectively. Meanwhile, the PI3K/protein kinase B (Akt) pathway-related proteins were also detected by Western blot. The proliferation, migration, angiogenesis, the mRNA and protein expression of VEGF and the protein expression of p-PI3K and p-AKT in HMEC-1 cells were increased after treated with mir-27b inhibitor. Meanwhile, the proliferation, migration, and the protein expression of collagen I, collagen III, α-SMA, MMP1, p-PI3K, and p-AKT in BJ cells were increased after treated with mir-27b inhibitor. However, the angiogenesis and fibroblast activation of mir-27b inhibitor was reversed by LY294002, and the activate effect to PI3K/Akt pathway was also inhibited. Down-regulation of mir-27b could promote angiogenesis and fibroblast activation, and its mechanism is related to activate PI3K/Akt signaling pathway.