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Published on: June 6, 2014
Identification of apoptotic proteins in thyroid gland from patients with Graves' disease and Hashimoto's thyroiditis
A Bossowski1, B Czarnocka, K Bardadin
12nd Department of Children's Diseases, Medical University of Bialystok, Bialystok, Poland. abossowski@hotmail.com
Abstract:
Apoptosis, i.e. natural programmed cell death, is a physiological phenomenon indispensable for normal functioning of the organism. The signal to apoptosis can be started practically in any cell. Disturbances in the apoptosis regulation determine the essential link of the pathogenesis of many diseases, including autoimmune thyroid disorders. The aim of the study was to assess the expression of Fas/FasL and caspase eight in the tissues of the thyroid gland in patients with Graves' disease (GD), non-toxic nodular goiter (NTNG) and Hashimoto's thyroiditis (HT). The analysis of Fas/FasL expression was performed by western blot and immunohistochemical investigation with DAB-visualization and Mayer's hematoxylin staining. Caspase-8 expression in thyroid follicular cells was assayed by western blot method. Identification of the proapoptotic proteins FasL and Fas exhibited their pronounced expression in the thyroid tissue in GD patients (++; ++) and HT (+++; +++) as compared to the NTNG group (0/+; 0/+). Among the study groups, the expression of caspase-8 was revealed in band 55 kDa from patients with autoimmune thyroid diseases. In GD patients, the percentage of thyrocytes with FasL expression correlated positively with TRAb (R = 0.58, p < 0.02). However, no such correlations were noted in HT or non-toxic multinodular goiter. There were no significant correlations between thyroid hormones and the percentage of thyrocytes with Fas and FasL expression. In conclusion, our findings suggest that the changes in the expression of apoptotic molecules on the surface of T lymphocytes and thyroid follicular cells in patients with autoimmune thyroid disorders reflect their substantial involvement in the pathogenesis of GD and HT. In addition, analysis of Fas/FasL and caspase-8 expression in thyroid tissue may indicate the disease activity and immunological phenotype.
Insights
Apoptosis, or programmed cell death, is crucial for health. This study found increased expression of Fas/FasL and caspase-8 in Graves' disease and Hashimoto's thyroiditis, suggesting their role in autoimmune thyroid disease pathogenesis.
Area of Science:
- Endocrinology
- Immunology
- Cell Biology
Background:
- Apoptosis (programmed cell death) is vital for organism function.
- Dysregulation of apoptosis is implicated in the pathogenesis of various diseases, including autoimmune thyroid disorders.
- Understanding apoptosis in thyroid tissue is key to understanding thyroid disease.
Purpose of the Study:
- To evaluate the expression of Fas/FasL and caspase-8 in thyroid tissue from patients with Graves' disease (GD), non-toxic nodular goiter (NTNG), and Hashimoto's thyroiditis (HT).
- To investigate the correlation between apoptotic molecule expression and disease activity markers.
- To elucidate the role of apoptosis in the pathogenesis of autoimmune thyroid diseases.
Main Methods:
- Western blot and immunohistochemical analysis were used to assess Fas/FasL expression.
- Western blot was employed to assay caspase-8 expression in thyroid follicular cells.
- Patients with GD, NTNG, and HT were included in the study.
Main Results:
- Proapoptotic proteins FasL and Fas showed significantly higher expression in thyroid tissue of GD and HT patients compared to NTNG patients.
- Caspase-8 expression was detected in patients with autoimmune thyroid diseases.
- In GD patients, FasL expression in thyrocytes positively correlated with TRAb levels, but not with thyroid hormones.
Conclusions:
- Altered expression of apoptotic molecules (Fas/FasL, caspase-8) in thyroid follicular cells and T lymphocytes is involved in the pathogenesis of GD and HT.
- Assessing Fas/FasL and caspase-8 expression in thyroid tissue may serve as an indicator of disease activity and immunological phenotype in autoimmune thyroid disorders.
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