Affiliation:
1. Department of Medical Rehabilitation, I. Horbachevsky Ternopil National Medical University, Majdan Voli 1,
Ternopil, 46001, Ukraine
2. Department of Microbiology, Virology, and Immunology, I. Horbachevsky Ternopil National
Medical University, Majdan Voli 1, Ternopil, 46001, Ukraine
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.
Objective:
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.
Conclusions:
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.
Publisher
Bentham Science Publishers Ltd.
Subject
Pharmaceutical Science,Biotechnology
Cited by
1 articles.
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