miR ‐128‐3p inhibits high‐glucose‐induced peritoneal mesothelial cells fibrosis via PAK2 / SyK / TGF ‐β1 axis

This is the authors' abstract. We don't add key points for this paper.

AIM: To elucidate the mechanism of miR-128-3p in peritoneal fibrosis (PF). METHODS: Peritoneal mesothelial cells (PMCs) were dealt with high glucose (HG) for 3 days. The expressions of miR-128-3p, p21-activated kinase 2 (PAK2), spleen tyrosine kinase (SyK), and transforming growth factor-β1 (TGF-β1) were detected with quantitative real-time reverse transcription polymerase chain reaction. The levels of IL-1β, TNF-α, IL-6, and monocyte chemotactic protein-1 in supernatant were measured by ELISA. Proteins of TGF-β1, SyK, PAK2, α-SMA, collagen I, vimentin, ERK/AP-1, and IκBα/NF-κB pathway related proteins were measured by Western blot. The correlation between miR-128-3p and PAK2 was found by bioinformatics analysis and luciferase reporter gene analysis. RESULTS: miR-128-3p was decreased while PAK2, SyK, and TGF-β1 were increased in HG-induced PMCs. Moreover, miR-128-3p inhibited HG-induced fibrosis and inflammation in PMCs by targeting PAK2. PAK2 activated SyK, which induced TGF-β1 expression through ERK/AP-1 and IκBα/NF-κB pathways to promote HG-induced fibrosis of PMCs. CONCLUSION: miR-128-3p inhibited HG-induced PMCs fibrosis via PAK2/SyK/TGF-β1 axis.