Details

Autor(en) / Beteiligte

• Sacristán-Gómez, Pablo
• Serrano-Somavilla, Ana
• Castro-Espadas, Lía
• Sánchez de la Blanca Carrero, Nuria
• Sampedro-Núñez, Miguel
• Muñoz-De-Nova, José Luis
• Molina-Jiménez, Francisca
• Rosell, Alejandra
• Marazuela, Mónica
• Martínez-Hernández, Rebeca

Titel

Evaluation of Epithelial-Mesenchymal Transition Markers in Autoimmune Thyroid Diseases

Ist Teil von

• International journal of molecular sciences, 2023-02, Vol.24 (4), p.3359

Ort / Verlag

Switzerland: MDPI AG

Erscheinungsjahr

2023

Quelle

MEDLINE

Beschreibungen/Notizen

• A state of chronic inflammation is common in organs affected by autoimmune disorders, such as autoimmune thyroid diseases (AITD). Epithelial cells, such as thyroid follicular cells (TFCs), can experience a total or partial transition to a mesenchymal phenotype under these conditions. One of the major cytokines involved in this phenomenon is transforming growth factor beta (TGF-β), which, at the initial stages of autoimmune disorders, plays an immunosuppressive role. However, at chronic stages, TGF- β contributes to fibrosis and/or transition to mesenchymal phenotypes. The importance of primary cilia (PC) has grown in recent decades as they have been shown to play a key role in cell signaling and maintaining cell structure and function as mechanoreceptors. Deficiencies of PC can trigger epithelial-mesenchymal transition (EMT) and exacerbate autoimmune diseases. A set of EMT markers (E-cadherin, vimentin, α-SMA, and fibronectin) were evaluated in thyroid tissues from AITD patients and controls through RT-qPCR, immunohistochemistry (IHC), and western blot (WB). We established an in vitro TGF-β-stimulation assay in a human thyroid cell line to assess EMT and PC disruption. EMT markers were evaluated in this model using RT-qPCR and WB, and PC was evaluated with a time-course immunofluorescence assay. We found an increased expression of the mesenchymal markers α-SMA and fibronectin in TFCs in the thyroid glands of AITD patients. Furthermore, E-cadherin expression was maintained in these patients compared to the controls. The TGF-β-stimulation assay showed an increase in EMT markers, including vimentin, α-SMA, and fibronectin in thyroid cells, as well as a disruption of PC. The TFCs from the AITD patients experienced a partial transition to a mesenchymal phenotype, preserving epithelial characteristics associated with a disruption in PC, which might contribute to AITD pathogenesis.