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1 Chair of Endocrinology, II Faculty of Medicine, University La Sapienza, Rome, Italy
2 Centro Ricerca AFaR, Ospedale San Pietro FBF, Via Cassia, 600, 00189 Rome, Italy
3 Oncology and Hematology Department, ISS, Rome, Italy
(Requests for offprints should be addressed to S Misiti; Email: silvia.misiti{at}uniroma1.it)
It has recently been recognized that thyroid hormones may rapidly generate biological responses by non-genomic mechanisms that are unaffected by inhibitors of transcription and translation. The signal transduction pathways underlying these effects are just beginning to be defined. We demonstrated that thyroid hormone T3 rapidly induces Akt activation in pancreatic ß cells rRINm5F and hCM via thyroid hormone receptor (TR) ß1. The phosphorylation of Akt was T3 specific and dependent. Coimmunoprecipitation and colocalization experiments revealed that the phosphatidylinositol 3 kinase (PI3K) p85
subunit and the thyroid receptor ß1 were able to form a complex at the cytoplasmic level in both the cell lines, suggesting that a ‘cytoplasmic TRß1’ was implicated. Moreover, we evidenced that T3 treatment was able to induce kinase activity of the TRß1-associated PI3K. The silencing of TRß1 expression through RNAi confirmed this receptor to be crucial for the T3-induced activation of Akt. This action involved a T3-induced nuclear translocation of activated Akt, as demonstrated by confocal immunofluorescence. In summary, T3 is able to specifically activate Akt in the islet ß cells rRINm5F and hCM through the interaction between TRß1 and PI3K p85, demonstrating the involvement of TRß1 in this novel T3 non-genomic action in islet ß cells.
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