Regulation and tissue distribution of the human sodium iodide symporter gene

R. A. Ajjan, Nor Azmi Kamaruddin, M. Crisp, P. F. Watson, M. Ludgate, A. P. Weetman

Research output: Contribution to journalArticle

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Abstract

OBJECTIVE: Iodide uptake by the thyroid gland is mediated by the sodium iodide symporter (NIS). In the present report, we have analysed the factors that modulate human NIS mRNA expression and iodide uptake in primary thyroid follicular cell (TFC) cultures. In addition, NIS mRNA tissue distribution was investigated. METHODS: Primary thyroid follicular cell cultures were treated with human recombinant TSH with or without cytokines for 72h. Subsequently, NIS gene expression and iodide uptake were analysed using reverse transcription-polymerase chain reaction (RT-PCR) and 125I uptake, respectively. Human tissue samples were investigated for NIS gene expression using both RT-PCR and Northern blotting. RESULTS: Human TSH increased both NIS gene expression and iodide uptake in TFC cultures in a dose-dependent manner. Using concentrations of 0.1 U/l of hTSH, a minor increase in NIS gene expression was detected without a detectable increase in iodide uptake. IL- 1α, TNFα and IFNγ at concentrations of 105 U/l all inhibited TSH-induced NIS gene expression and iodide uptake. In these experiments, there was a good correlation between NIS mRNA expression and iodide uptake. Using RT-PCR higher levels of NIS mRNA were detected in Graves' disease (GD) compared to multi-nodular goitre tissue samples. Stomach and salivary gland tissue also expressed NIS mRNA, whereas low levels were found in the mammary gland and extraocular muscle tissue. No expression was detected in the ovary, oesophagus, colon, extraocular fat or skin. In contrast, Northern blot analysis failed to detect NIS in stomach, salivary gland, intestinal fat or non-toxic multi-nodular goitre tissue samples, although this was present in GD thyroid tissue. CONCLUSION: TSH upregulates sodium iodide symporter gene expression and iodide uptake in primary thyroid follicular cell cultures, and this induction is modulated by cytokines. Variable levels of sodium iodide symporter mRNA are present in different tissue samples, with high expression evident in Graves' disease thyroid tissue.

Original languageEnglish
Pages (from-to)517-523
Number of pages7
JournalClinical Endocrinology
Volume49
Issue number4
DOIs
Publication statusPublished - 1998
Externally publishedYes

Fingerprint

Iodides
Tissue Distribution
Gene Expression
Messenger RNA
Genes
Graves Disease
Cell Culture Techniques
Reverse Transcription
Nodular Goiter
Thyroid Gland
Salivary Glands
Northern Blotting
Polymerase Chain Reaction
Oculomotor Muscles
Stomach
Thyrotropin Alfa
Fats
Cytokines
sodium-iodide symporter
Human Mammary Glands

ASJC Scopus subject areas

  • Endocrinology

Cite this

Regulation and tissue distribution of the human sodium iodide symporter gene. / Ajjan, R. A.; Kamaruddin, Nor Azmi; Crisp, M.; Watson, P. F.; Ludgate, M.; Weetman, A. P.

In: Clinical Endocrinology, Vol. 49, No. 4, 1998, p. 517-523.

Research output: Contribution to journalArticle

Ajjan, R. A. ; Kamaruddin, Nor Azmi ; Crisp, M. ; Watson, P. F. ; Ludgate, M. ; Weetman, A. P. / Regulation and tissue distribution of the human sodium iodide symporter gene. In: Clinical Endocrinology. 1998 ; Vol. 49, No. 4. pp. 517-523.
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AU - Ajjan, R. A.

AU - Kamaruddin, Nor Azmi

AU - Crisp, M.

AU - Watson, P. F.

AU - Ludgate, M.

AU - Weetman, A. P.

PY - 1998

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N2 - OBJECTIVE: Iodide uptake by the thyroid gland is mediated by the sodium iodide symporter (NIS). In the present report, we have analysed the factors that modulate human NIS mRNA expression and iodide uptake in primary thyroid follicular cell (TFC) cultures. In addition, NIS mRNA tissue distribution was investigated. METHODS: Primary thyroid follicular cell cultures were treated with human recombinant TSH with or without cytokines for 72h. Subsequently, NIS gene expression and iodide uptake were analysed using reverse transcription-polymerase chain reaction (RT-PCR) and 125I uptake, respectively. Human tissue samples were investigated for NIS gene expression using both RT-PCR and Northern blotting. RESULTS: Human TSH increased both NIS gene expression and iodide uptake in TFC cultures in a dose-dependent manner. Using concentrations of 0.1 U/l of hTSH, a minor increase in NIS gene expression was detected without a detectable increase in iodide uptake. IL- 1α, TNFα and IFNγ at concentrations of 105 U/l all inhibited TSH-induced NIS gene expression and iodide uptake. In these experiments, there was a good correlation between NIS mRNA expression and iodide uptake. Using RT-PCR higher levels of NIS mRNA were detected in Graves' disease (GD) compared to multi-nodular goitre tissue samples. Stomach and salivary gland tissue also expressed NIS mRNA, whereas low levels were found in the mammary gland and extraocular muscle tissue. No expression was detected in the ovary, oesophagus, colon, extraocular fat or skin. In contrast, Northern blot analysis failed to detect NIS in stomach, salivary gland, intestinal fat or non-toxic multi-nodular goitre tissue samples, although this was present in GD thyroid tissue. CONCLUSION: TSH upregulates sodium iodide symporter gene expression and iodide uptake in primary thyroid follicular cell cultures, and this induction is modulated by cytokines. Variable levels of sodium iodide symporter mRNA are present in different tissue samples, with high expression evident in Graves' disease thyroid tissue.

AB - OBJECTIVE: Iodide uptake by the thyroid gland is mediated by the sodium iodide symporter (NIS). In the present report, we have analysed the factors that modulate human NIS mRNA expression and iodide uptake in primary thyroid follicular cell (TFC) cultures. In addition, NIS mRNA tissue distribution was investigated. METHODS: Primary thyroid follicular cell cultures were treated with human recombinant TSH with or without cytokines for 72h. Subsequently, NIS gene expression and iodide uptake were analysed using reverse transcription-polymerase chain reaction (RT-PCR) and 125I uptake, respectively. Human tissue samples were investigated for NIS gene expression using both RT-PCR and Northern blotting. RESULTS: Human TSH increased both NIS gene expression and iodide uptake in TFC cultures in a dose-dependent manner. Using concentrations of 0.1 U/l of hTSH, a minor increase in NIS gene expression was detected without a detectable increase in iodide uptake. IL- 1α, TNFα and IFNγ at concentrations of 105 U/l all inhibited TSH-induced NIS gene expression and iodide uptake. In these experiments, there was a good correlation between NIS mRNA expression and iodide uptake. Using RT-PCR higher levels of NIS mRNA were detected in Graves' disease (GD) compared to multi-nodular goitre tissue samples. Stomach and salivary gland tissue also expressed NIS mRNA, whereas low levels were found in the mammary gland and extraocular muscle tissue. No expression was detected in the ovary, oesophagus, colon, extraocular fat or skin. In contrast, Northern blot analysis failed to detect NIS in stomach, salivary gland, intestinal fat or non-toxic multi-nodular goitre tissue samples, although this was present in GD thyroid tissue. CONCLUSION: TSH upregulates sodium iodide symporter gene expression and iodide uptake in primary thyroid follicular cell cultures, and this induction is modulated by cytokines. Variable levels of sodium iodide symporter mRNA are present in different tissue samples, with high expression evident in Graves' disease thyroid tissue.

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