Transcriptional activity of TGFβ1 and its receptors genes in thyroid gland
| Autor: | Bogdan Marek, Elżbieta Morawiec-Szymonik, Wanda Foltyn, Lucyna Siemińśka, Danuta Niedziołka-Zielonka, Mariusz Nowak, Anna Fila-Danilow, Beata Kos-Kudła, Michał Seemann, Dariusz Kajdaniuk, Urszula Mazurek, Joanna Głogowska-Szeląg, Anna Marek |
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| Rok vydání: | 2015 |
| Předmět: |
Adult
Male Pathology medicine.medical_specialty Transcription Genetic endocrine system diseases Endocrinology Diabetes and Metabolism medicine.medical_treatment Graves' disease Thyroid Gland Biology Transforming Growth Factor beta1 Pathogenesis Endocrinology Fibrosis medicine Humans Receptor Thyroid Thyroidectomy Middle Aged medicine.disease Thyroid Diseases Real-time polymerase chain reaction Cytokine medicine.anatomical_structure Female Receptors Transforming Growth Factor beta |
| Zdroj: | Endokrynologia Polska. |
| ISSN: | 2299-8306 0423-104X |
| DOI: | 10.5603/ep.a2016.0045 |
| Popis: | 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) |
| Databáze: | OpenAIRE |
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