Transcription Factors and Regulators Pathway-focused Genes Expression Analysis in Patients with Different Forms of Thyroid Pathology

Abstract

Background: Autoimmune thyroiditis (AIT), a T cell-mediated organ-specific disorder, and transcription factors have a critical role in the regulation of immune responses, especially in the fate of T-helper cells.

Objectives: This study aims to investigate changes in the gene expression profile of transcription factors and regulators in patients with different forms of thyroid pathology.

Methods: We used the pathway-specific real-time PCR array (Neurotrophins and Receptors RT2 Profiler PCR Array, QIAGEN, Germany) to identify and verify transcription factors and regulators pathway-focused genes expression in peripheral white blood cells of patients with postoperative hypothyroidism, hypothyroidism as a result of AIT and AIT with elevated serum and antithyroglobulin (anti-Tg) and anti-thyroid peroxidase (anti-TPO) antibodies.

Results: It was shown that in patients with postoperative hypothyroidism FOS, NR1I2, STAT4, and TP53 significantly increased their expression, whereas the expression of STAT1, STAT2, and STAT3 decreased. In patients with hypothyroidism as a result of AIT, we have found increased expression of NR1I2, STAT2, and STAT3. In contrast, the expression of STAT1 and TP53 decreased. FOS and STAT4 mRNAs did not change their expression. In patients with AIT and elevated serum anti-Tg and anti-TPO antibodies, the expression of FOS and NR1I2 reduced, whereas the mRNA level of STAT3 increased. STAT1, STAT2, and STAT4 mRNAs did not change their expression. MYC did not change its expression in all groups of patients.

Conclusion: The results of this study demonstrate that autoimmune thyroiditis and hypothyroidism affect the mRNA-level expression of transcription factors and regulators genes in a gene-specific manner and that these changes to genes expression can be one of the triggers of autoimmune inflammation progression in the thyroid gland.

Keywords: STAT1; STAT2; Transcription factors; autoimmune thyroiditis; hypothyroidism; mRNA.