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Updated: Mar 18, 2026

An Ex vivo Culture System to Study Thyroid Development
Published on: June 6, 2014
Transcriptional activity of TGFβ1 and its receptors genes in thyroid gland
Dariusz Kajdaniuk1, Anna Marek, Bogdan Marek
1Department of Pathophysiology and Endocrinology, School of Medicine with the Division of Dentistry in Zabrze, Medical University of Silesia, Katowice. kaj.darius@interia.pl.
Introduction:
Determination of gene-candidates' profile expression responsible for fibrosis, immunosuppression, angiogenesis, and neoplasia processes in the pathogenesis of thyroid gland disease.
Material And Methods:
Sixty-three patients underwent thyroidectomy: 27 with non-toxic nodular goitre (NG), 22 with toxic nodular goitre (TNG), six with papillary cancer (PTC), and eight with Graves' disease (GD). In thyroid tissues, transcriptional activity of TGFbeta1 and its receptors TGFbetaRI, TGFbetaRII, and TGFbetaRIII genes were assessed using RT-qPCR (Reverse Transcriptase Quantitative Polymerase Chain Reaction). Molecular analysis was performed in tissues derived from GD and from the tumour centre (PTC, NG, TNG) and from peripheral parts of the removed lobe without histopathological lesions (tissue control). Control tissue for analysis performed in GD was an unchanged tissue derived from peripheral parts of the removed lobe of patients surgically treated for a single benign tumour.
Results/Conclusions:
Strict regulation observed among transcriptional activity of TGFb1 and their receptor TGFbetaRI-III genes in control tissues is disturbed in all pathological tissues - it is completely disturbed in PTC and GD, and partially in NG and TNG. Additionally, higher transcriptional activity of TGFb1 gene in PTC in comparison with benign tissues (NG, GD) and lower expression of mRNA TGFbRII (than in TNG, GD) and mRNA TGFbetaRIII than in all studied benign tissues (NG, TNG, GD) suggests a pathogenetic importance of this cytokine and its receptors in PTC development. In GD tissue, higher transcriptional activity of TGFbetaRII and TGFbetaRIII genes as compared to other pathological tissues was observed, indicating a participation of the receptors in the pathomechanism of autoimmune thyroid disease (AITD). TGFbeta1 blood concentrations do not reflect pathological processes taking place in thyroid gland. (Endokrynol Pol 2016; 67 (4): 375-382).
Insights
Gene expression of transforming growth factor beta 1 (TGF-β1) and its receptors is altered in various thyroid diseases. This suggests their role in thyroid cancer and autoimmune thyroid disease pathogenesis.
Area of Science:
- Endocrinology
- Molecular Biology
- Oncology
Background:
- Thyroid gland diseases involve complex processes like fibrosis, immunosuppression, angiogenesis, and neoplasia.
- Understanding the gene expression profiles of these processes is crucial for disease pathogenesis.
- The transforming growth factor beta 1 (TGF-β1) signaling pathway is implicated in various cellular functions relevant to thyroid disease.
Purpose of the Study:
- To determine the gene expression profiles of TGF-β1 and its receptors (TGF-βRI, TGF-βRII, TGF-βRIII) in different thyroid pathologies.
- To investigate the role of TGF-β1 signaling in the pathogenesis of non-toxic nodular goitre (NG), toxic nodular goitre (TNG), papillary thyroid cancer (PTC), and Graves' disease (GD).
- To assess the correlation between gene expression in thyroid tissue and TGF-β1 blood concentrations.
Main Methods:
- Thyroidectomy was performed on 63 patients with NG, TNG, PTC, and GD.
- Transcriptional activity of TGF-β1 and its receptors was quantified using Reverse Transcriptase Quantitative Polymerase Chain Reaction (RT-qPCR).
- Gene expression analysis was conducted on tumor tissues, surrounding non-tumorous tissues, and control tissues.
Main Results:
- Transcriptional regulation of TGF-β1 and its receptors was disrupted in all pathological thyroid tissues compared to controls.
- Papillary thyroid cancer (PTC) showed significantly higher TGF-β1 gene activity than benign tissues.
- Graves' disease (GD) tissues exhibited higher TGF-βRII and TGF-βRIII gene activity compared to other pathological tissues.
Conclusions:
- The strict regulation of TGF-β1 and its receptor gene expression is disturbed in various thyroid pathologies, particularly in PTC and GD.
- TGF-β1 signaling pathway components play a significant role in the pathogenesis of papillary thyroid cancer.
- Altered expression of TGF-β receptors in Graves' disease suggests their involvement in the pathomechanism of autoimmune thyroid disease.
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