MiR-140-5p upregulation suppressed β-glycerophosphate-induced vascular smooth muscle cell calcification via targeting TLR4. (4th May 2022)

• Record Type: Journal Article
• Authors: Zhang, Fan; Li, Jingxing; Gu, Chengxiong; Zhang, Haibo
• Is Part Of: Immunopharmacology and immunotoxicology. Volume 44:Number 3(2022)
• Page Start: 295
• Page End: 305
• Publication Date: 2022-05-04
• Subjects: Vascular calcification -- microRMA-140-5p -- β-glycerophosphate -- vascular smooth muscle cells -- Toll like receptor 4; Immunopharmacology -- Periodicals; Immunotoxicology -- Periodicals; Antibody-toxin conjugates -- Periodicals; Immunology -- Periodicals; 615.37
• DOI: 10.1080/08923973.2022.2043896
• Languages: English
• ISSNs: 0892-3973

Abstract

Abstract: Background: The role and function of microRNA (miRNA, miR)-140-5p in the calcification of vascular smooth muscle cells (VSMCs) have been explored in this study. Methods: The calcium nodules formed in transfected and β-glycerophosphate (β-GP)-treated VSMCs were observed using Alizarin Red S staining, and alkaline phosphatase (ALP) activity was determined. VSMC apoptosis was detected with flow cytometry assay. The target gene of miR-140-5p was predicted and confirmed with dual-luciferase reporter assay. Relative expressions of miR-140-5p, toll like receptor 4 (TLR4) and vascular calcification-related proteins (α-smooth muscle actin, α-SMA; Msh Homeobox 2, MSX2; bone morphogenetic protein 2, BMP2; Kruppel-like factor 4, KLF4; Runt-related transcription factor 2, RUNX2) were measured through quantitative real time polymerase chain reaction (qRT-PCR) and western blot. Results: MiR-140-5p upregulation reversed the effects of β-GP on downregulating miR-140-5p and α-SMA expressions, enhancing ALP activity, calcium nodule formation and cell apoptosis, and upregulating levels of MSX2, BMP2, KLF4 and RUNX2. TLR4 was the target of miR-140-5p, and offset the effects of miR-140-5p on β-GP-induced VSMCs. Conclusions: MiR-140-5p upregulation represses β-GP-induced calcification of VSMCs via targeting TLR4, providing a potential therapeutic method for vascular calcification.