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Related Experiment Videos

Nitric oxide stimulates cyclic GMP in human thyrocytes

L J Millatt1, R Jackson, B C Williams

  • 1Department of Cellular and Molecular Sciences, St George's Hospital Medical School, London UK.

Journal of Molecular Endocrinology
|April 1, 1993
PubMed
Summary

Sodium nitroprusside increases cyclic GMP (cGMP) in human thyroid cells via nitric oxide. This pathway is independent of cyclic AMP (cAMP) and thyroid hormone secretion.

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Area of Science:

  • Endocrinology
  • Molecular Biology
  • Cell Signaling

Background:

  • Sodium nitroprusside (SNP) releases nitric oxide (NO), a vasodilator that activates guanylate cyclase, increasing cyclic guanosine monophosphate (cGMP).
  • The role of NO-cGMP signaling in human thyroid cells (thyrocytes) is not fully understood.

Purpose of the Study:

  • To investigate the effect of SNP on cGMP production in primary human thyrocytes and a human thyroid cell line (SGHTL-189).
  • To determine the relationship between NO-cGMP signaling and cAMP production or thyroid hormone secretion in these cells.

Main Methods:

  • Primary human thyrocytes and SGHTL-189 cells were treated with SNP.
  • cGMP and cyclic adenosine monophosphate (cAMP) levels were measured.
  • The effect of methylene blue (NO scavenger) and forskolin (cAMP stimulator) was assessed.

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  • Triiodothyronine secretion was measured.

    • Main Results:

    • SNP dose-dependently increased cGMP in both cell types, with maximum response above 10 microM.
    • Methylene blue inhibited SNP-induced cGMP production, confirming the role of NO.
    • SNP did not affect cAMP production or basal/TSH-stimulated triiodothyronine secretion.
    • Forskolin reduced SNP-stimulated cGMP production, but this was not linked to cAMP levels.

    Conclusions:

    • Nitric oxide-mediated cGMP production occurs in human thyroid cells.
    • This pathway is distinct from cAMP signaling and does not influence thyroid hormone secretion.
    • SNP represents a tool to study NO-cGMP signaling in the thyroid.