TRAIL and DR5 Promote Thyroid Follicular Cell Apoptosis in Iodine Excess-Induced Experimental Autoimmune Thyroiditis in NOD Mice |
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Authors: | Xiujie Yu Lanying Li Qingxin Li Xiaoyi Zang Zebing Liu |
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Institution: | (1) Key Lab of Hormone and Institute of Endocrinology, Metabolic Disease Hospital, Tianjin Medical University of Tianjin, 127#, Tianjin Medical University of Tianjin, 300070 Tianjin, China; |
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Abstract: | Death receptor-mediated apoptosis has been implicated in target organ destruction in patients with chronic autoimmune thyroiditis.
Several apoptosis signaling pathways, such as Fas ligand and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL),
have been shown to be active in thyroid cells and may be involved in destructive thyroiditis. Thyroid toxicity of iodide excess
has been demonstrated in animals fed with an iodide-rich diet, but its pathogenic role remains unclear. The effects of excessive
iodine on TRAIL and its death receptor expression in thyroid were investigated. Experimental autoimmune thyroiditis (EAT)
was induced by excessive iodine and thyroglobulin (Tg) in non-obese diabetic mice. The expression of TRAIL and its death receptor
DR5 was detected by immunofluorescence staining. Following administration of excessive iodine alone, Tg, and excessive iodine
combined with Tg, TRAIL-positive cells appear not only in follicular cells but also in lymphocytes infiltrated in the thyroid,
whereas DR5-positive cells appear only in follicular cells. Large numbers of CD3-positive cells and a few CD22-positive cells
were detected in thyroid. A great amount of follicular cells were labeled specifically by terminal deoxynucleotide transferase-mediated
deoxynucleotide triphosphate nick-end labeling assay. Taken together, our results suggest that excessive iodine could induce
TRAIL and DR5 abnormal expression in thyroid. TRAIL band with DR5 to promote follicular cells apoptosis thus mediate thyroid
destruction in EAT. |
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