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

Author:

Soleimani Ali Akbar1,Shokri Nafiseh2,Elahimanesh Mohammad2,Mohammadi Payam2,Parvaz Najmeh2,Bakhshandeh Masoomeh2,Najafi Mohammad234ORCID

Affiliation:

1. Department of Clinical Biochemistry, Faculty of Medicine Tehran University of Medical Sciences Tehran Iran

2. Department of Clinical Biochemistry, Faculty of Medicine Iran University of Medical Sciences Tehran Iran

3. Cellular and Molecular Research Center Iran University of Medical Sciences Tehran Iran

4. Microbial Biotechnology Center Iran University of Medical Sciences Tehran Iran

Abstract

AbstractBackgroundMetformin (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 β‐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.

Funder

Iran University of Medical Sciences

Publisher

Wiley

Subject

Endocrinology, Diabetes and Metabolism

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