3,5,3鈥?Triiodothyronine (T₃) stimulates cell proliferation through the activation of the PI3K/Akt pathway and reactive oxygen species (ROS) production in chick embryo hepatocytes

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• 作者：Davide Gnocchi^a ; ^{davide.gnocchi@uniroma1.it} ; Silvia Leoni^a ; Sandra Incerpi^b ; Giovannella Bruscalupi^a
• 关键词：3 ; 5 ; 3&prime ; -Triiodothyronine (T3) ; Nongenomic effects ; Integrin 伪v尾3 ; PI3K/Akt pathway ; Reactive oxygen species (ROS) ; Chick embryo hepatocytes
• 刊名：Steroids
• 出版年：2012
• 期刊代码：142_0039128x
• 类别：bio
• 出版时间：May, 2012
• 卷：77
• 期：6
• 页码：589-595
• 文件大小：426 K

摘要

Thyroid hormones (THs) have a wide variety of essential roles in vertebrates, ranging from the regulation of key metabolic processes to cell proliferation and apoptosis. The classical mechanism of action of THs is genomic; 3,5,3鈥?triiodothyronine (T₃) binds to specific nuclear receptors (TRs) and modifies the expression of specific genes.

Recently, a new category of mechanisms, termed nongenomic, has been discovered for T₃. These mechanisms include, among others, the rapid activation of signal transduction pathways, such as PI3K/Akt and MAPK, which eventually lead to cell proliferation. These effects are mediated in some cell types by a plasma membrane receptor, identified as integrin 伪v尾3, and in other cell types by cytoplasmic TR尾1.

The aim of this work was to analyze the effect of T₃ on the cell growth of chick embryo hepatocytes at two different stages of development, 14 and 19 days, and to determine the activation of the signal transduction pathways, focusing on the potential involvement of a plasma membrane receptor and the possible participation of PI3K/Akt and reactive oxygen species (ROS).

Our results clearly show that T₃ stimulates cell proliferation at both stages of development through the activation of the PI3K/Akt pathway and the production of small amounts of ROS, which operate as effective second messengers. Moreover, we prove that these effects are not initiated at the plasma membrane receptor for T₃.