Identification of chosen apoptotic (TIAR and TIA-1) markers expression in thyroid tissues from adolescents with immune and non-immune thyroid diseases.

Abstract

Abstract:The aim of this study was to estimate sodium iodide symporter (NIS) and thyroid peroxidase (TPO) expression in thyrocytes from patients with GD and no-toxic multinodular goitre (NTMG) in relationship with apoptotic (TIAR and TIA-1) markers. The investigation was performed on thyroid cells isolated from postoperation thyroid tissues from 15 patients aged 12-21 years old with GD and 15 cases aged 13-21 years old with NTMG. Detection of NIS and TPO was performed by immunohistochemistry. Analysis of apoptotic markers in thyroid tissues was performed using antibodies to TIAR and TIA-1 by Western Blot and immunohistochemistry. Identification of proapoptotic TIAR and TIA-1 molecules in the thyroid tissues revealed a higher expression of both proteins in patients with Graves' disease (+++; +, respectively) in comparison to patients with NTNG (+; 0). In addition, TIAR expression was detected in three bands [p50, p42, p38 (kDa)] and TIA-1 in two bands [p22, p17 (kDa)]. using Western Blot test in patients with thyroid autoimmune diseases. In patients with NTNG expression of both apoptotic proteins was lower and identified in single bands: 42 (kDa) for TIAR and 17 (kDa) for TIA-1. The analysis of expression of NIS and TPO in thyroid follicular cells was higher in patients with Graves' disease in compared to their detection in patients with NTMG. In addition, degree of thyroid antigen expression positive correlated with amount of proapoptotic markers (TIAR, p<0.001; TIA-1, p<0.025 for NIS; TIAR, p<0.012 for TPO). We conclude that elevated expression of NIS and TPO in Graves' disease is associated with higher stimulation and activation of apoptosis in thyroid follicular cells during autoimmune process.

Peripheral blood lymphocyte apoptosis and its relationship with thyroid function tests in adolescents with hyperthyroidism due to Graves' disease

“…The course of GD is associated with the inflow of lymphocytes to the thyroid gland and dysregulation of the immune system characterized by reaction to thyroid antigens (peroxidase, thyroglobulin, TSH receptors and Na+/I- symporter). After activation they shift to the inflamed thyroid gland, thus leading to the production of cytokines which can stimulate activity of thyrocytes and increase expression of intracellular proapoptotic markers such as TIAR and TIA-1 [18]. Other authors emphasize that in GD, the Th2 cytokine profile is associated with upregulation of antiapoptotic molecules, rendering the thyrocytes but not the infiltrating lymphocytes immune from apoptosis [19].…”

Identification of Classifiers for Increase or Decrease of Thyroid Peroxidase Activity in the FTC-238/hTPO Recombinant Cell Line

“…The biological processes associated with the 362 prediction markers included the WD domain, embryonic development, apoptosis regulation, and Ras protein signal transduction. WD domains have been implicated in signal transduction and transcription regulation, and play roles in the cell cycle and apoptosis. , The disruption of TPO activity in Graves’ disease is related to increased stimulation of apoptosis in thyroid follicular cells . Propylthiouracil-induced hypothyroidism due to the inhibition of TPO activity results in TH deficiency, as well as alterations in oxidative stress and the consequent apoptosis of cerebellum cells during neonatal brain development .…”

T-Cell Intracellular Antigen 1-Like Protein in Physiology and Pathology

“…Similarly, TIAR gain-of-function models in HEK293 cells trigger an apoptotic phenotype in a p53 pathway-associated cellular response [ 95 ]. In the same vein, the C. elegans TIA1/TIAR homolog, TIAR-1/TIAR-2, is required for germ cell apoptosis [ 105 , 110 ], and a correlation exists between thyroid disease and excessive apoptosis in thyroid tissues associated with elevated TIAR expression [ 111 ]. Regardless, there is a commonality between TIA1 and TIAR since their complete inactivation in HEK293 cells leads to mitotic catastrophe and cell death [ 38 ].…”