Short-term effects of triiodothyronine on thyroid hormone receptor alpha by PI3K pathway in adipocytes, 3T3-L1

• Published in: Arquivos brasileiros de endocrinologia e metabologia Vol. 58; no. 8; pp. 833 - 837
• Main Authors: Oliveira, Miriane de, Olimpio, Regiane Marques Castro, Sibio, Maria Teresa De, Moretto, Fernanda Cristina Fontes, Luvizotto, Renata de Azevedo Mello, Nogueira, Célia Regina
• Format: Journal Article
• Language: English
• Published: Brazil Sociedade Brasileira de Endocrinologia e Metabologia 01-11-2014
• Subjects: 3T3-L1 Cells; Adipocytes - drug effects; Adipocytes - metabolism; Animals; Cell Differentiation; Chromones - pharmacology; ENDOCRINOLOGY & METABOLISM; Gene Expression - genetics; Genes, erbA - drug effects; Mice; Morpholines - pharmacology; Phosphatidylinositol 3-Kinase - metabolism; RNA, Messenger - metabolism; Thyroid Hormone Receptors alpha - genetics; Thyroid Hormone Receptors alpha - metabolism; Time Factors; Triiodothyronine - pharmacology; TRα; Triiodothyronine; adipócitos; PI3K; Triiodotironina; adipocytes
• ISSN: 0004-2730; 1677-9487; 1677-9487; 0004-2730
• DOI: 10.1590/0004-2730000003295

The present study aimed to examine the effects of thyroid hormone (TH), more precisely triiodothyronine (T3), on the modulation of TH receptor alpha (TRα) mRNA expression and the involvement of the phosphatidyl inositol 3 kinase (PI3K) signaling pathway in adipocytes, 3T3-L1, cell culture.
It was examined the involvement of PI3K pathway in mediating T3 effects by treating 3T3-L1 adipocytes with physiological (P=10nM) or supraphysiological (SI =100 nM) T3 doses during one hour (short time), in the absence or the presence of PI3K inhibitor (LY294002). The absence of any treatment was considered the control group (C). RT-qPCR was used for mRNA expression analyzes. For data analyzes ANOVA complemented with Tukey's test was used at 5% significance level.
T3 increased TRα mRNA expression in P (1.91±0.13, p<0.001), SI (2.14±0.44, p<0.001) compared to C group (1±0.08). This increase was completely abrogated by LY294002 in P (0.53±0.03, p<0.001) and SI (0.31±0.03, p<0.001). To examine whether TRα is directly induced by T3, we used the translation inhibitor cycloheximide (CHX). The presence of CHX completely abrogated levels TRα mRNA in P (1.15±0.05, p>0.001) and SI (0.99±0.15, p>0.001), induced by T3.
These results demonstrate that the activation of the PI3K signaling pathway has a role in T3-mediated indirect TRα gene expression in 3T3-L1 adipocytes.