Influence of Signal Transducer and Activator of Transcription-1 Signaling on Thyroid Morphology and Function

被引：13

作者：

Kimura, Hiroaki J.

Rocchi, Roberto

Landek-Salgado, Melissa A.

Suzuki, Koichi ^{[3
]}

Chen, Cindy Y.

Kimura, Miho

Rose, Noel R. ^{[2
]}

Caturegli, Patrizio ^{[1
,2
]}

机构：

[1] Johns Hopkins Sch Med, Dept Pathol, Johns Hopkins Med Inst, Baltimore, MD 21205 USA

[2] Johns Hopkins Bloomberg Sch Publ Hlth, Feinstone Dept Mol Microbiol & Immunol, Baltimore, MD 21205 USA

[3] Natl Inst Infect Dis, Dept Bioregulat, Leprosy Res Ctr, Tokyo 1890002, Japan

来源：

ENDOCRINOLOGY | 2009年 / 150卷 / 07期

基金：

美国国家卫生研究院;

关键词：

GROWTH-FACTOR-BETA; INTERFERON-GAMMA; IFN-GAMMA; TRANSFORMING GROWTH-FACTOR-BETA-1; CHEMOKINE EXPRESSION; GENE-TRANSCRIPTION; STAT1; CELLS; HYPOTHYROIDISM; KINASE;

D O I：

10.1210/en.2008-1769

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Interferon (IFN)-gamma has been involved in the pathogenesis of Hashimoto thyroiditis. It is a cytokine released by infiltrating mononuclear cells that mediates its actions mainly through signal transducer and activator of transcription-1 (STAT1) but also through other transcription factors. To dissect the effect of IFN gamma on thyroid morphology and function, we crossed transgenic mice that express IFN gamma specifically in the thyroid gland to mice deficient in STAT1. Lack of STAT1 ameliorated the abnormal thyroid morphology and the primary hypothyroidism typical of IFN gamma transgenic mice but not the suppressed iodine accumulation. Interestingly, lack of STAT1 alone decreased iodine accumulation, seemingly through expression of TGF beta. These results indicate that STAT1 is required to mediate some but not all of the phenotypic changes induced by IFN gamma and that it also regulates iodine accumulation via TGF beta signaling. (Endocrinology 150: 3409-3416, 2009)

引用

页码：3409 / 3416

页数：8

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