title: Transcriptional activity of TGFβ1 and its receptors genes in thyroid gland.
abstract: BACKGROUND
  Determination of gene-candidates' profile expression responsible for fibrosis, immunosuppression, angiogenesis, and neoplasia processes in the pathogenesis of thyroid gland disease.
  
  
  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.
  
  
  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).
authors.affiliation: Department of Pathophysiology and Endocrinology, School of Medicine with the Division of Dentistry in Zabrze, Medical University of Silesia, Katowice. kaj.darius@interia.pl.
authors.forename: Dariusz
authors.initials: D
authors.lastname: Kajdaniuk
authors.forename: Anna
authors.initials: A
authors.lastname: Marek
authors.forename: Bogdan
authors.initials: B
authors.lastname: Marek
authors.forename: Urszula
authors.initials: U
authors.lastname: Mazurek
authors.forename: Anna
authors.initials: A
authors.lastname: Fila-Daniłow
authors.forename: Wanda
authors.initials: W
authors.lastname: Foltyn
authors.forename: Elżbieta
authors.initials: E
authors.lastname: Morawiec-Szymonik
authors.forename: Lucyna
authors.initials: L
authors.lastname: Siemińśka
authors.forename: Mariusz
authors.initials: M
authors.lastname: Nowak
authors.forename: Joanna
authors.initials: J
authors.lastname: Głogowska-Szeląg
authors.forename: Danuta
authors.initials: D
authors.lastname: Niedziołka-Zielonka
authors.forename: Michał
authors.initials: M
authors.lastname: Seemann
authors.forename: Beata
authors.initials: B
authors.lastname: Kos-Kudła
mesh_terms: D000328:Adult; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D018125:Receptors, Transforming Growth Factor beta / Q000235:genetics*; D013959:Thyroid Diseases / Q000378:metabolism*; D013961:Thyroid Gland / Q000378:metabolism*; D014158:Transcription, Genetic; D053773:Transforming Growth Factor beta1 / Q000235:genetics*
chemical_list: D018125:Receptors, Transforming Growth Factor beta; C508960:TGFB1 protein, human; D053773:Transforming Growth Factor beta1
keywords: Graves’ disease; TGFbeta1; nodular goiter; papillary cancer; thyroid; transforming growth factor beta 1