title: Analysis of correlation between the process of thyroid fibrosis and TGFB1 gene expression level in fine-needle aspiration biopsy (FNAB) thyroid specimens collected from patients with Hashimoto's thyroiditis and non-toxic goitre.
abstract: Transforming growth factor beta 1 (TGFB1) stimulates the production of various extracellular matrix components; at the same time, it inhibits matrix degradation. These actions of TGFB1 contribute to tissue repair, however, an altered expression of TGFB1 can be a causative factor of fibrosis processes, including thyroid fibrosis which follows chronic thyroiditis. The aim of our study was to examine a potential correlation between TGFB1 gene expression level in fine-needle aspiration biopsy (FNAB) thyroid specimens and fibrosis of the thyroid gland in two types of thyroid lesions. Fibrosis of the thyroid tissue was assessed, based on the expression levels of fibrosis-associated genes (COL1A1 and COL3A1) in thyroid FNAB samples, on the FNAB specimen cellularity and other features of the tissue fibrosis assessed during cytological examination, as well as on the size of thyroid gland and its function. Following routine cytological examination, 63 thyroid FNAB specimens, received from patients with Hashimoto's thyroiditis (HT, n=30) and non-toxic goitre (NTG, n=33), were quantitatively evaluated regarding TGFB1, COL1A1 and COL3A1 expression level by real-time PCR in the ABI PRISM 7500 Sequence Detection System. The obtained results showed statistically significant differences regarding the expression level (RQ) of TGFB1 and of COL1A1 genes between the groups with HT and with NTG (higher expression in HT group). No significant differences, concerning the expression level of COL3A1 gene, were observed for the studied groups (HT vs. NTG). In HT group statistically significant correlation was found between TGFB1 gene and COL3A1 gene expression levels (p<0.05). The correlation in question might suggest excessive extracellular matrix deposition and could--possibly--contribute to thyroid fibrosis mechanism in the course of chronic thyroiditis.
authors.affiliation: 1Department of Endocrinology and Metabolic Diseases, Medical University of Lodz, Lodz, Poland.
authors.forename: A
authors.initials: A
authors.lastname: Cyniak-Magierska
authors.forename: J
authors.initials: J
authors.lastname: Januszkiewicz-Caulier
authors.forename: E
authors.initials: E
authors.lastname: Brzeziańska
authors.forename: A
authors.initials: A
authors.lastname: Lewiński
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D044963:Biopsy, Fine-Needle; D024042:Collagen Type I / Q000235:genetics*; D000090602:Collagen Type I, alpha 1 Chain; D024061:Collagen Type III / Q000235:genetics; D005260:Female; D005355:Fibrosis; D015870:Gene Expression; D006042:Goiter / Q000175:diagnosis / Q000235:genetics / Q000473:pathology*; D050031:Hashimoto Disease / Q000175:diagnosis / Q000235:genetics / Q000473:pathology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D013961:Thyroid Gland / Q000473:pathology*; D053773:Transforming Growth Factor beta1 / Q000235:genetics*; D055815:Young Adult
chemical_list: C439971:COL3A1 protein, human; D024042:Collagen Type I; D000090602:Collagen Type I, alpha 1 Chain; D024061:Collagen Type III; C508960:TGFB1 protein, human; D053773:Transforming Growth Factor beta1