Objective: Nitric oxide (NO) induces morphological and functional alterations in primary cultured thyroid cells.
The aim of this paper was to analyze the direct influence of a long-termexposition to NO on parameters of thyroid hormone biosynthesis in FRTL-5 cells. Design: Cells were treated with the NO donor sodium nitroprusside (SNP)
for 24?72 h. Main Outcome: SNP (50?500 mmol=L) reduced iodide uptake in a concentration-dependent manner.
The inhibition of iodide uptake increased progressively with time and matched nitrite accumulation. SNP inhibited thyroperoxidase (TPO) and thyroglobulin (TG) mRNA expression in a concentration-dependent manner. SNP enhanced 30,50-cyclic guanosine monophosphate (cGMP) production. 30,50-cyclic adenosine phosphate (cAMP)
generation was reduced by a high SNP concentration after 48 h. 8-Bromoguanosine 30,50-cyclic monophosphate
(8-Br-cGMP), a cGMP analog, inhibited iodide uptake as well as TPO and TG mRNA expression. The cGMPdependent protein kinase (cGK) inhibitor KT-5823 reversed SNP or 8-Br-cGMP-inhibited iodide uptake. Thyroidstimulating hormone pretreatment for 24?48 h prevented SNP-reduced iodide uptake although nitrite levels remained unaffected. Conclusion: These findings favor a long-term inhibitory role of the NO=cGMP pathway on
parameters of thyroid hormone biosynthesis. A novel property of NO to inhibit TPO and TG mRNA expression is supported. The NO action on iodide uptake could involve cGK mediation. The long-term inhibition of steps of thyroid hormonogenesis by NO could be of interest in thyroid pathophysiology.
The aim of this paper was to analyze the direct influence of a long-termexposition to NO on parameters of thyroid
hormone biosynthesis in FRTL-5 cells. Design: Cells were treated with the NO donor sodium nitroprusside (SNP)
for 24?72 h. Main Outcome: SNP (50?500 mmol=L) reduced iodide uptake in a concentration-dependent manner.
The inhibition of iodide uptake increased progressively with time and matched nitrite accumulation. SNP inhibited thyroperoxidase (TPO) and thyroglobulin (TG) mRNA expression in a concentration-dependent manner. SNP enhanced 30,50-cyclic guanosine monophosphate (cGMP) production. 30,50-cyclic adenosine phosphate (cAMP)
generation was reduced by a high SNP concentration after 48 h. 8-Bromoguanosine 30,50-cyclic monophosphate
(8-Br-cGMP), a cGMP analog, inhibited iodide uptake as well as TPO and TG mRNA expression. The cGMPdependent protein kinase (cGK) inhibitor KT-5823 reversed SNP or 8-Br-cGMP-inhibited iodide uptake. Thyroidstimulating hormone pretreatment for 24?48 h prevented SNP-reduced iodide uptake although nitrite levels remained unaffected. Conclusion: These findings favor a long-term inhibitory role of the NO=cGMP pathway on
parameters of thyroid hormone biosynthesis. A novel property of NO to inhibit TPO and TG mRNA expression is supported. The NO action on iodide uptake could involve cGK mediation. The long-term inhibition of steps of thyroid hormonogenesis by NO could be of interest in thyroid pathophysiology.
for 24?72 h. Main Outcome: SNP (50?500 mmol=L) reduced iodide uptake in a concentration-dependent manner.
The inhibition of iodide uptake increased progressively with time and matched nitrite accumulation. SNP inhibited thyroperoxidase (TPO) and thyroglobulin (TG) mRNA expression in a concentration-dependent manner. SNP enhanced 30,50-cyclic guanosine monophosphate (cGMP) production. 30,50-cyclic adenosine phosphate (cAMP)
generation was reduced by a high SNP concentration after 48 h. 8-Bromoguanosine 30,50-cyclic monophosphate
(8-Br-cGMP), a cGMP analog, inhibited iodide uptake as well as TPO and TG mRNA expression. The cGMPdependent protein kinase (cGK) inhibitor KT-5823 reversed SNP or 8-Br-cGMP-inhibited iodide uptake. Thyroidstimulating hormone pretreatment for 24?48 h prevented SNP-reduced iodide uptake although nitrite levels remained unaffected. Conclusion: These findings favor a long-term inhibitory role of the NO=cGMP pathway on
parameters of thyroid hormone biosynthesis. A novel property of NO to inhibit TPO and TG mRNA expression is supported. The NO action on iodide uptake could involve cGK mediation. The long-term inhibition of steps of thyroid hormonogenesis by NO could be of interest in thyroid pathophysiology.
The inhibition of iodide uptake increased progressively with time and matched nitrite accumulation. SNP inhibited
thyroperoxidase (TPO) and thyroglobulin (TG) mRNA expression in a concentration-dependent manner. SNP
enhanced 30,50-cyclic guanosine monophosphate (cGMP) production. 30,50-cyclic adenosine phosphate (cAMP)
generation was reduced by a high SNP concentration after 48 h. 8-Bromoguanosine 30,50-cyclic monophosphate
(8-Br-cGMP), a cGMP analog, inhibited iodide uptake as well as TPO and TG mRNA expression. The cGMPdependent protein kinase (cGK) inhibitor KT-5823 reversed SNP or 8-Br-cGMP-inhibited iodide uptake. Thyroidstimulating hormone pretreatment for 24?48 h prevented SNP-reduced iodide uptake although nitrite levels remained unaffected. Conclusion: These findings favor a long-term inhibitory role of the NO=cGMP pathway on
parameters of thyroid hormone biosynthesis. A novel property of NO to inhibit TPO and TG mRNA expression is supported. The NO action on iodide uptake could involve cGK mediation. The long-term inhibition of steps of thyroid hormonogenesis by NO could be of interest in thyroid pathophysiology.
generation was reduced by a high SNP concentration after 48 h. 8-Bromoguanosine 30,50-cyclic monophosphate
(8-Br-cGMP), a cGMP analog, inhibited iodide uptake as well as TPO and TG mRNA expression. The cGMPdependent protein kinase (cGK) inhibitor KT-5823 reversed SNP or 8-Br-cGMP-inhibited iodide uptake. Thyroidstimulating hormone pretreatment for 24?48 h prevented SNP-reduced iodide uptake although nitrite levels remained unaffected. Conclusion: These findings favor a long-term inhibitory role of the NO=cGMP pathway on
parameters of thyroid hormone biosynthesis. A novel property of NO to inhibit TPO and TG mRNA expression is supported. The NO action on iodide uptake could involve cGK mediation. The long-term inhibition of steps of thyroid hormonogenesis by NO could be of interest in thyroid pathophysiology.
(8-Br-cGMP), a cGMP analog, inhibited iodide uptake as well as TPO and TG mRNA expression. The cGMPdependent
protein kinase (cGK) inhibitor KT-5823 reversed SNP or 8-Br-cGMP-inhibited iodide uptake. Thyroidstimulating
hormone pretreatment for 24?48 h prevented SNP-reduced iodide uptake although nitrite levels
remained unaffected. Conclusion: These findings favor a long-term inhibitory role of the NO=cGMP pathway on
parameters of thyroid hormone biosynthesis. A novel property of NO to inhibit TPO and TG mRNA expression is supported. The NO action on iodide uptake could involve cGK mediation. The long-term inhibition of steps of thyroid hormonogenesis by NO could be of interest in thyroid pathophysiology.
parameters of thyroid hormone biosynthesis. A novel property of NO to inhibit TPO and TG mRNA expression
is supported. The NO action on iodide uptake could involve cGK mediation. The long-term inhibition of steps of
thyroid hormonogenesis by NO could be of interest in thyroid pathophysiology.
