Identification of apoptotic proteins in thyroid gland from patients with Graves' disease and Hashimoto's thyroiditis The work was presented at XVI Symposium of Polish Society of Pediatric Endocrinology (PSPE) in Bialowieza, 28-30.09.2006 and at the Conference of European Society of Pediatric Endocrinology (ESPE), 30.06.2006-03.07.2006, Rotterdam, Holland
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 disease...
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Veröffentlicht in: | Autoimmunity (Chur, Switzerland) Switzerland), 2008-03, Vol.41 (2), p.163-173 |
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Format: | Artikel |
Sprache: | eng |
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Zusammenfassung: | 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 55kDa from patients with autoimmune thyroid diseases. In GD patients, the percentage of thyrocytes with FasL expression correlated positively with TRAb (R=0.58, p |
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ISSN: | 0891-6934 1607-842X |
DOI: | 10.1080/08916930701727749 |