Beta arrestin-related signalling axes are influenced by dexamethasone and metformin in vascular smooth muscle cells cultured in high glucose condition

BackgroundMetformin (Met) and dexamethasone (Dexa) are known to reduce blood sugar levels and anti-inflammatory effects, respectively. Based on the acceleration of atherosclerosis process in diabetes, the beta-arrestin 2 (BARR2) gene and protein expression levels were evaluated in vascular smooth muscle cells (VSMCs) treated with Met and Dexa in high glucose conditions in this study.Methods and MaterialsHuman VSMCs were cultured in Dulbecco's Modified Eagle Medium/Nutrient Mixture F-12 (DMEM-F12) medium and, were treated with different values of Met (1 mM, 5 mM and 7 mM) and Dexa (10-7 M, 10-6 M and 10-5 M) in 24- and 48-h periods. The BARR2 gene and protein expression levels were identified with RT-qPCR and western blotting techniques, respectively. The signalling axes were predicted from gene network made using Cytoscape software and, were annotated with Gene Ontology.ResultsThe BARR2 gene and protein expression levels reduced in VSMCs treated with Dexa and Met after 24- and 48-h periods. These results were more changed after 48 h. Furthermore, many BARR2-related signalling axes were found from the network genes.ConclusionMet and Dexa suppressed the BARR2 protein and gene expression levels in the VSMCs. Moreover, the gene network suggested some the cellular signalling axes related to BARR2 that may be affected by Met and Dexa. The study results showed that metformin (Met) similar to dexamethasone (Dexa) suppresses the beta-arrestin 2 (BARR2) protein and gene expression levels in the vascular smooth muscle cells (VSMCs). Furthermore, the gene network data suggested that BARR2-related signalling axes might affect many cellular signalling pathways by Met and Dexa. However, more studies are needed to find the roles of Met and Dexa in these signalling pathways.image