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首页> 外文学位 >Signaling pathways employed by thyroid stimulating hormone to induce interleukin-6 release from human and 3T3-L1 adipocytes.
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Signaling pathways employed by thyroid stimulating hormone to induce interleukin-6 release from human and 3T3-L1 adipocytes.

机译：甲状腺刺激激素用于诱导人和3T3-L1脂肪细胞中白介素6释放的信号通路。

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摘要

Subclinical hypothyroidism, a condition characterized by elevated thyroid stimulating hormone (TSH) levels, is a risk factor for cardiovascular disease (CVD). Adipose tissue contributes significantly to the circulating levels of interleukin-6 (IL-6), an atherogenic and pro-inflammatory cytokine. Adipose cells express TSH receptors and are responsive to TSH. The overall hypothesis of my Ph.D. project is that TSH acts on adipose cells to stimulate the release of IL-6.;I first showed that in 3T3-Ll cells, TSH induces IL-6 release from differentiated adipocytes, but not from precursor cells (preadipocytes). Differentiated 3T3-Ll adipocytes increased IL-6 release in response to TSH via activation of the cAMP-dependent protein kinase (PKA) pathway. Following analysis of the TSH effect on 3T3-Ll adipose cell line, I proceeded to examine the effect of TSH on human primary adipose cells.;For the abdominal subcutaneous depot, I found that preadipocytes did not release IL-6 in response to TSH, but their differentiated adipocytes counterparts were TSH-responsive. In contrast, for the omental depot, I showed that neither preadipocytes nor the differentiated adipocytes increased IL-6 release in response to TSH.;Signaling studies on the human abdominal subcutaneous differentiated adipocytes revealed that TSH activates the nuclear factor kappa-B pathway to induce IL-6 release. Furthermore, PKA activation by TSH does not result in increased NF-kappaB signaling.;In this thesis, I studied TSH-induced IL-6 release and the related signaling mechanisms using the mouse 3T3-Ll adipose cell line. I also evaluated human primary adipose cells, and examined the influence of stage of differentiation and fat depot localization on the effect of TSH on IL-6 release.;To demonstrate that TSH could act in an extra-thyroidal fashion in vivo, I analyzed serum IL-6levels in thyroidectomized patients with a past history of thyroid cancer undergoing recombinant human (rh)TSH administration. Injection with rhTSH increased IL-6 serum levels, supporting the notion that TSH has extra-thyroidal actions in vivo.;In summary, this thesis demonstrates that TSH is capable of regulating inflammatory responses on adipose cells and of elevating IL-6, a biomarker of inflammation, in the circulation of thyroidectomized patients.
机译：亚临床甲状腺功能减退症是一种以甲状腺刺激激素（TSH）水平升高为特征的疾病，是心血管疾病（CVD）的危险因素。脂肪组织对动脉粥样硬化和促炎性细胞因子白细胞介素6（IL-6）的循环水平有重要贡献。脂肪细胞表达TSH受体并对TSH有反应。我的博士学位的总体假设我的研究首先表明在3T3-L1细胞中，TSH诱导分化的脂肪细胞（而不是前体细胞（前脂肪细胞））释放IL-6。通过激活cAMP依赖性蛋白激酶（PKA）途径，分化的3T3-L1脂肪细胞增加了对TSH的IL-6释放。在分析了TSH对3T3-L1脂肪细胞系的作用后，我继续研究了TSH对人原代脂肪细胞的作用。​​对于腹部皮下贮藏库，我发现前脂肪细胞不响应TSH释放IL-6，但它们分化的脂肪细胞对应物对TSH反应。相比之下，对于网膜贮库，我发现前脂肪细胞和分化的脂肪细胞均未增加对TSH的反应中的IL-6释放。 IL-6释放。此外，TSH激活PKA不会导致NF-κB信号转导增加。在本文中，我使用小鼠3T3-L1脂肪细胞系研究了TSH诱导的IL-6释放及其相关信号转导机制。我还评估了人类原代脂肪细胞，并研究了分化阶段和脂肪储库定位对TSH对IL-6释放的影响。为了证明TSH可以在体内以甲状腺外的方式起作用，我分析了血清接受重组人（rh）TSH给药的，有甲状腺癌病史的甲状腺切除患者中的IL-6水平。注射rhTSH会增加IL-6的血清水平，支持TSH在体内具有甲状腺外作用的观点。总之，本论文证明TSH能够调节脂肪细胞上的炎症反应并能升高生物标志物IL-6。炎症，在甲状腺切除患者的循环中。

著录项

  • 作者

    Antunes, Tayze Tatiana.;

  • 作者单位

    University of Ottawa (Canada).;

  • 授予单位 University of Ottawa (Canada).;
  • 学科 Chemistry Biochemistry.
  • 学位 Ph.D.
  • 年度 2009
  • 页码 146 p.
  • 总页数 146
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

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