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

Abstract 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.