title: [Analysis of intracellular proapoptotic (Bax, Bak) and antiapoptotic (Bcl-2, Bcl-XL) proteins expression in thyrocytes from young patients with immune and non-immune thyroid disorders].
abstract: Apoptosis one of the form of programmed cell death is a physiological occurrence, requisite to the correct function of every organism. This is an active process that proceeds with a participation of the cellular metabolism embracing the activation of genes and the synthesis of proteins. The signal to apoptosis can be started practically in every cell of our organism. Disturbances of the apoptosis regulation determine the essential link of the pathogenesis of many diseases, including autoimmune thyroid disorders. The aim of this study was to estimate the expression of proapoptotic (Bax, Bak) and antiapoptotic (Bcl-2, Bcl-XL) proteins in thyroid tissues from 12 patients with Graves' disease (GD), 10 with non-toxic nodular goitre (NTNG) and 10 with toxic nodular goitre (TNG). Criteria for qualification of Graves' patients: large goitre, ophthalmopathy, TRAb > 5 U/L, positive titre of anti-TPO and anti-TG antibodies and concentration of TSH <0.45 microIU/mL more the 2-3 months from onset of the disease. Detection of apoptotic proteins in thyroid follicular cells was performed by Western Blot. These analysis was confirmed by immunohistochemistry using monoclonal antibodies in DAB chromogene visuality and marked by Mayer's haematoxylin. Identification of antiapoptotic Bcl-2 and Bcl-XL molecules in the thyroid follicular cells revealed a higher expression of both proteins in patients with Graves' disease (+++; ++, respectively) in comparison to patients with NTNG (++/+; +) and TNG (++; +). The detection of proapoptotic molecules showed higher expression of Bak (++/+) and Bax (+) in Graves' thyroid tissues while Bax was in trace amount in NTNG (0/+) and TNG (0/+). We conclude that alteration in the expression of antiapoptotic and proapoptotic proteins on surface of thyroid follicular cells may play a role in the pathogenesis of thyroid autoimmune disorders. In addition, suppression of apoptosis in Graves' disease led to predominance for proliferation of thyroid follicular cells which is responsible for goitre formation.
authors: ll Klinika Chorób Dzieci AM w Białymstoku.
authors: Artur
authors: A
authors: Bossowski
authors: Barbara
authors: B
authors: Czarnocka
authors: Krzysztof
authors: K
authors: Bardadin
authors: Mirosława
authors: M
authors: Urban
authors: Marek
authors: M
authors: Niedziela
authors: Jacek
authors: J
authors: Dadan
mesh_terms: D000293:Adolescent; D000328:Adult; D051017:Apoptosis Regulatory Proteins / Q000378:metabolism*; D001327:Autoimmune Diseases / Q000097:blood; D002648:Child; D003593:Cytoplasm / Q000378:metabolism; D005260:Female; D006044:Goiter, Nodular / Q000276:immunology / Q000378:metabolism; D006111:Graves Disease / Q000276:immunology / Q000378:metabolism; D006801:Humans; D018828:Immunoglobulins, Thyroid-Stimulating / Q000097:blood; D007150:Immunohistochemistry; D007453:Iodide Peroxidase / Q000097:blood*; D008297:Male; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D013959:Thyroid Diseases / Q000276:immunology* / Q000378:metabolism*; D013961:Thyroid Gland / Q000166:cytology* / Q000378:metabolism*; D013971:Thyrotoxicosis / Q000276:immunology / Q000378:metabolism; D050998:bcl-2 Homologous Antagonist-Killer Protein / Q000378:metabolism; D051028:bcl-2-Associated X Protein / Q000378:metabolism; D051020:bcl-X Protein / Q000378:metabolism
chemical_list: D051017:Apoptosis Regulatory Proteins; D018828:Immunoglobulins, Thyroid-Stimulating; D019253:Proto-Oncogene Proteins c-bcl-2; D050998:bcl-2 Homologous Antagonist-Killer Protein; D051028:bcl-2-Associated X Protein; D051020:bcl-X Protein; D007453:Iodide Peroxidase