Interleukin-1 inhibits thyrotrophin-induced human thyroglobulin gene expression

Yamashita, Shunichi; Kimura, Hironori; Ashizawa, Kiyoto; Nagayama, Yuji; Hirayu, Hideshi; Izumi, Motomori; Nagataki, Shigenobu

doi:10.1677/joe.0.1220177

Cited by 48 publications

(22 citation statements)

References 33 publications

(41 reference statements)

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“…There have been several reports that IL-1 has stimulatory or inhibitory effects on the growth of human thyroid carcinoma cell lines (Kimura et al 1992, Zeki et al 1993, Inokuchi et al 1995, Yip et al 1995, although it is believed to have an inhibitory effect on human thyroid-specific gene expression , Ashizawa et al 1989. In the present study, we confirmed that IL-1 has a stimulatory effect on the growth of NIM1 cells and an inhibitory effect on the growth of NPA cells.…”

Section: Discussionsupporting

confidence: 85%

Interleukin-1alpha regulates G1 cell cycle progression and arrest in thyroid carcinoma cell lines NIM1 and NPA

Zeki¹,

Morimoto²,

Arao³

et al. 1999

Journal of Endocrinology

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This study provides the first report that the same cytokine (interleukin-1 (IL-1)) can induce opposite effects on cyclin-dependent kinases (Cdks) and Cdk inhibitors (Cdkis) in the G 1 phase even in the same type of cancer cells (papillary thyroid carcinoma cells). Cell cycle analysis revealed an increase in NIM1 cells and a decrease in NPA cells in the S and G 2 +M phases after treatment with IL-1 . The addition of IL-1 to NIM1 cells reduced the expression of p16 and p21 protein and induced the expression of Cdk2 and Cdk4 protein, which leads to the phosphorylation of retinoblastoma protein. The addition of IL-1 to NPA cells induced the expression of p27 protein and reduced the expression of Cdk2 protein, which leads to induction of p107 protein expression. It is of interest that p21 protein expression was not observed in NPA cells. These results suggest that several Cdks and Cdkis play a regulatory role in the G 1 cell cycle progression and arrest induced by IL-1 in thyroid carcinoma cell lines.

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Section: Discussionsupporting

confidence: 85%

Interleukin-1alpha regulates G1 cell cycle progression and arrest in thyroid carcinoma cell lines NIM1 and NPA

Zeki¹,

Morimoto²,

Arao³

et al. 1999

Journal of Endocrinology

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“…TSH was rather inhibitory on the cytokine(s)-induced MCP-1 expression. In contrast, the expression of TG, a thyroid-specific protein, mRNA and protein was remarkably stimulated by TSH and this TSH-dependent up-regulation of TG expression was completely blocked by a co-administration of IL-I as reported previously [27]. Furthermore, over 95% of the cultured cells incubated with TSH alone were positively stained with anti-TG antibody (data not shown).…”

Section: Discussionsupporting

confidence: 72%

Expression of monocyte chemoattractant protein‐1 mRNA and protein in cultured human thyrocytes

et al. 1996

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Monocytes as well as lymphocytes infiltrate in the stroma of thyroid tissue in autoimmune and destructive thyroiditis. Monocyte chemoattractant protein-1 (MCP-I) is a cytokine that attracts T-lymphocytes as well as monocytes. Using human thyrocytes in primary cultures, we show that expression of MCP-1 mRNA and protein is remarkably stimulated by both interleukin-1 (IL-1) and tumor necrosis factor-~ (TNF-ct), and also that interferon-T (IFN-~/) by itself is a weak stimulant but has a synergistic activity with either IL-1 or TNF-c¢, The finding indicates that MCP-1 can be produced by thyrocytes themselves, suggesting a possible role of thyrocytes on accumulation of monocytes and T-lymphocytes to the tissue from the blood in autoimmune and destructive thyroiditis.

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“…Unlike IFN␥, IL-1␤ did not impair TSH-induced Tg expression or DNA synthesis in WRT cells. These results differ somewhat from those reported in human cells, where IL-1␤ impaired Tg expression stimulated by TSH (39,40; reviewed in Ref. 41).…”

Section: Discussioncontrasting

confidence: 92%

Differential Effects of Acute and Chronic Exposure to Interferon-γ on Cyclic Adenosine 3′,5′-Monophosphate Response Element-Regulated Gene Expression1

et al. 2000

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TSH stimulates proliferation and maintains differentiated function in thyroid follicular cells. The mitogenic activity and the stimulatory effects of TSH on thyroid-specific gene expression are impaired by interferon-␥ (IFN␥); however, the mechanisms for these effects have not been elucidated in detail. We examined the effects of IFN␥ on acute responses to TSH in rat thyroid cells. IFN␥ did not impair TSH-stimulated p70/p85 ribosomal protein S6 kinase (p70/ p85s6k) activity or cAMP response element (CRE)-regulated gene expression, although it inhibited DNA synthesis and thyroglobulin expression, effects measured over a more prolonged time course than those on kinase activity and reporter gene expression. Unexpectedly, when cells were chronically exposed to IFN␥, CRE-lacZ promoter activity was decreased, whereas other cAMP-mediated signals, such as p70/p85s6k activity and CRE-binding protein phosphorylation, were unaffected. Activating protein-1-regulated promoters were also impaired by IFN␥ treatment, but with kinetics that differed from those of CRE-regulated promoters. Neither acute nor chronic treatment with interleukin-1␤ impaired cAMP signaling, indicating that the effects of IFN␥ are specific. These studies identify CRE-and activating protein-1-regulated promoters as targets of IFN␥ in thyroid cells and fibroblasts. IFN␥-mediated inhibition of these promoters, in addition to those containing thyroid-specific transcription factor-1-binding sites, may contribute to the profound effects of IFN␥ on thyroid cells. (Endocrinology 141: 606 -614, 2000) T SH COORDINATELY regulates proliferation and differentiated function in thyroid follicular cells. TSH stimulates the expression of thyroid-specific genes, including the TSH receptor (TSHR) (reviewed in Ref. 1), thyroglobulin (Tg) (2-5), thyroid peroxidase (5, 6), iodothyronine 5-deiodinase (7), and the sodium-iodide symporter (8, 9). Cytokines, including interferon-␥ (IFN␥), interleukin-1␤ (IL-1␤), and tumor necrosis factor-␣, are believed to participate in the development and progression of thyroid autoimmunity. IFN␥ increases the autoantigenicity of thyrocytes by upregulating MHC class I expression (10) and by inducing aberrant expression of MHC class II antigens (11-17). Moreover, the expression of several genes under regulatory control by TSH is inhibited by IFN␥. In turn, TSH impairs IFN␥-stimulated Fas expression (18). In addition to opposing effects on gene expression, TSH and IFN␥ exert differential effects on proliferation, where IFN␥ has been shown to inhibit TSH-stimulated proliferation (12,19,20).Thyroid-specific transcription factor-1 (TITF-1; previously termed TTF-1) (21) has been identified as one molecular target of IFN␥ in FRTL-5 cells where IFN␥ decreases TITF-1 DNA-binding activity on the TSHR promoter (22). In human thyroid cells, IFN␥ activates a nuclear protein that binds to the Tg promoter and diminishes Tg expression (23). Given the multitude of the effects of IFN␥ on thyroid cells, it seems likely that there are additional mechan...

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Interleukin-1 inhibits thyrotrophin-induced human thyroglobulin gene expression

Cited by 48 publications

References 33 publications

Interleukin-1alpha regulates G1 cell cycle progression and arrest in thyroid carcinoma cell lines NIM1 and NPA

Interleukin-1alpha regulates G1 cell cycle progression and arrest in thyroid carcinoma cell lines NIM1 and NPA

Expression of monocyte chemoattractant protein‐1 mRNA and protein in cultured human thyrocytes

Differential Effects of Acute and Chronic Exposure to Interferon-γ on Cyclic Adenosine 3′,5′-Monophosphate Response Element-Regulated Gene Expression1

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