open access

Vol 67, No 4 (2016)
Original papers
Published online: 2016-06-10
Submitted: 2016-06-09
Accepted: 2016-06-09
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Transcriptional activity of TGFβ1 and its receptors genes in thyroid gland

Dariusz Kajdaniuk, Anna Marek, Bogdan Marek, Urszula Mazurek, Anna Fila-Daniłow, Wanda Foltyn, Elżbieta Morawiec-Szymonik, Lucyna Siemińśka, Mariusz Nowak, Joanna Głogowska-Szeląg, Danuta Niedziołka-Zielonka, Michał Seemann, Beata Kos-Kudła
DOI: 10.5603/EP.a2016.0045
·
Endokrynologia Polska 2016;67(4):375-382.

open access

Vol 67, No 4 (2016)
Original papers
Published online: 2016-06-10
Submitted: 2016-06-09
Accepted: 2016-06-09

Abstract

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)

Abstract

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)

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Keywords

TGFbeta1; transforming growth factor beta 1; thyroid; nodular goiter; papillary cancer; Graves’ disease;

About this article
Title

Transcriptional activity of TGFβ1 and its receptors genes in thyroid gland

Journal

Endokrynologia Polska

Issue

Vol 67, No 4 (2016)

Pages

375-382

Published online

2016-06-10

DOI

10.5603/EP.a2016.0045

Bibliographic record

Endokrynologia Polska 2016;67(4):375-382.

Keywords

TGFbeta1
transforming growth factor beta 1
thyroid
nodular goiter
papillary cancer
Graves’ disease

Authors

Dariusz Kajdaniuk
Anna Marek
Bogdan Marek
Urszula Mazurek
Anna Fila-Daniłow
Wanda Foltyn
Elżbieta Morawiec-Szymonik
Lucyna Siemińśka
Mariusz Nowak
Joanna Głogowska-Szeląg
Danuta Niedziołka-Zielonka
Michał Seemann
Beata Kos-Kudła

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