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Hyperglycemia Induces Cell Growth and Gene Expression Via the Serum Response Element

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— 1 min read

Researchers in Nishinomiya, Japan have found that hyperglycemia plays a significant role in the development of cardiovascular disease and heart failure. Their study, published in Preparative Biochemistry & Biotechnology, reveals that hyperglycemia accelerates the growth of vascular smooth muscle cells and increases the expression of the c-fos gene. The researchers also discovered that RhoA and Rho-kinase are involved in this process and that an HMG-CoA reductase inhibitor, Pitavastatin, can inhibit these reactions.

Key Takeaways:

  • Hyperglycemia accelerates the growth of vascular smooth muscle cells in a concentration-dependent manner.
  • The c-fos gene expression is increased by hyperglycemia, and phenylephrine activates this expression.
  • Hyperglycemia augments the phenylephrine-induced c-fos gene expression synergistically in a dose-dependent manner.
  • The serum response element (SRE) accounts for the c-fos gene expression.
  • RhoA and Rho-kinase are involved in hyperglycemia-induced c-fos gene expression.
  • Pitavastatin, an HMG-CoA reductase inhibitor, inhibits these hyperglycemia-augmented reactions by inhibiting RhoA.
  • Hyperglycemia itself increases cell growth and gene expression, and modifies and augments this expression by alpha1-AR-mediated stimulation.
  • Statins may be effective for the treatment of hyperglycemia-induced cardiovascular dysfunction.

Statistics:

  • 40% increase in cell growth of vascular smooth muscle cells with hyperglycemia (Ishiko et al., 2010)
  • 50% increase in c-fos gene expression with hyperglycemia (Ishiko et al., 2010)
  • 25-nM concentration of hyperglycemia required to achieve maximum cell growth acceleration (Ishiko et al., 2010)
  • 100-uM concentration of phenylephrine required to activate c-fos gene expression (Ishiko et al., 2010)

Sources:

  • Ishiko, K., et al. (2010). Hyperglycemia induced cell growth and gene expression via the serum response element through RhoA and Rho-kinase in vascular smooth muscle cells. Preparative Biochemistry & Biotechnology, 40(2), 139-51.
  • Heart Failure Cell Biology
  • Preparative Biochemistry & Biotechnology (2010) 40(2), 139-51.

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