期刊
MOLECULAR AND CELLULAR ENDOCRINOLOGY
卷 337, 期 1-2, 页码 71-79出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mce.2011.02.001
关键词
Estrogen; Extracellular matrix; PC CL3 cells; Stromal cells; TGF-beta 1; Thyroid
资金
- Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq)
- Fundacao Carlos Chagas Filho de Amparo a Pesquisa do Estado do Rio de Janeiro (FAPERJ)
- Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES)
The higher prevalence of thyroid disease in women suggests that estrogen (E2) might be involved in the pathophysiology of thyroid dysfunction. To approach the question of the effect of stromal cells in the modulation of thyroid epithelial cells activity, we established and characterized a homogeneous stromal cell population (TS7 cells) of rat thyroid gland. These fibroblastic cells synthesize the cytoskeleton proteins a-smooth muscle actin and vimentin, produce basement membrane components and express the cytokine transforming growth factor beta 1 (TGF-beta 1). Here, we hypothesized that the effects of E2 on follicular thyroid cells are mediated by TGF-beta 1 synthesis and secretion by stromal cells (paracrine action). Thus we investigated the effect of E2 on TGF-beta 1 synthesis and its signaling pathway in TS7 cells. In addition, we analyzed the role of TGF-beta 1 signaling pathway as mediator of TS7-PC CU thyroid epithelial cells interactions. We report that TS7 stromal cells expressed alpha and beta estrogen receptors (ER alpha and ER beta). Further, both isoforms of TGF-beta 1 receptors, TGFRI and TGFRII, were also identified in TS7 cells, suggesting that these cells might be a target for this cytokine in vitro. Treatment of TS7 cells with E2 induced both synthesis and secretion of TGF-beta 1. This event was followed by phosphorylation of the transcription factor Smad2, a hallmark of TGF-beta 1 pathway activation. Co-culture of PC CL3 cells onto TS7 cells monolayers yielded round aggregates of PC CU cells surrounded by TS7 cells. TS7 cells induced a decrease in iodide uptake by PC CL3 cells, probably by a mechanism involving TGF-beta 1. Moreover, E2 affected synthesis and organization of the extracellular matrix (ECM) components, tenascin C and chondroitin sulfate, in these co-culture cells. Our results point to the TGF-beta 1/Smad-2 signaling pathway as a putative target of estrogen actions on thyroid stromal cells and contribute to understanding the interplay between stromal and follicular cells in thyroid physiology. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据