Focal adhesion kinase-related pathways may be suppressed by metformin in vascular smooth muscle cells in high glucose conditions

Endocrinol Diabetes Metab. 2022 Jul;5(4):e351. doi: 10.1002/edm2.351. Epub 2022 May 28.

Abstract

Introduction: Cardiovascular diseases are known as one of the important causes of death in patients with diabetes mellitus. Metformin is used as an oral medication for reducing blood sugar. In this study, the effects of metformin were investigated on the FAK gene expression levels, pFAK protein values, cell viability and migration rate of VSMCs in high glucose conditions.

Materials and methods: The FAK gene expression levels and pFAK protein values were evaluated in VSMCs treated with different doses of metformin (1, 5 and 7 mM), based on cell viability using RT-qPCR, western blotting and MTT techniques. The cellular migration was evaluated by scratch assay.

Results: The FAK gene expression levels reduced significantly in metformin-treated VSMCs at 24 h and 48 h periods (p < .0008 and p < .0001, respectively). The pFAK protein values reduced significantly at 24 h (5 mM and 7 mM metformin doses) and 48 h periods (p < .001). In agreement with pFAK protein values, cellular migration reduced significantly at 24 h and 48 h periods (p < .001).

Conclusion: The results showed that metformin may suppress the proliferation and migration of VSMCs via FAK-related pathways and may retard the progression of vessel stenosis in diabetes.

Keywords: FAK; VSMCs; high glucose; metformin; migration.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Focal Adhesion Protein-Tyrosine Kinases / metabolism
  • Glucose / metabolism
  • Glucose / pharmacology
  • Humans
  • Metformin* / pharmacology
  • Muscle, Smooth, Vascular* / metabolism
  • Myocytes, Smooth Muscle / metabolism

Substances

  • Metformin
  • Focal Adhesion Protein-Tyrosine Kinases
  • Glucose