Potassium iodide promotes the pyroptosis of thyroid follicular epithelial cells through the PARP1-NF-κB-NLRP3 inflammasome activation
10.3760/cma.j.cn311282-20210318-00176
- VernacularTitle:碘化钾通过诱导PARP1表达活化NF-κB/NLRP3炎症小体促进甲状腺滤泡细胞焦亡
- Author:
Mei LIU
1
;
Jing HUANG
;
Jun WANG
;
Shaobo HU
;
Shan LI
;
Chen XIONG
;
Fang LIU
;
Chunhui YUAN
;
Yuhai HU
;
Wenzao SUN
Author Information
1. 武汉市汉口医院检验科 430016
- Keywords:
Potassium iodide;
Thyroid follicular cell;
Pyroptosis;
PARP1;
Nuclear factor-κB;
NLRP3 inflammasome
- From:
Chinese Journal of Endocrinology and Metabolism
2021;37(9):820-829
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To explore the mechanism of potassium iodide-induced pyrolysis of thyroid follicular cells.Methods:Thyroid gland tissue was obtained from patients with thyroid cancer (TC) coexisting with Hashimoto′s thyroiditis, and the tumor-adjacent Hashimoto′s thyroiditis tissue was used as the control. ELISA was used to detect the concentration of the pyroptosis inflammatory cytokines interleukin (IL)-1β and IL-18 in the tissues, and Western blotting was used to detect the activation of gasdermin (GSDM) proteins, a biomarker for pyroptosis. Thyroid follicular cells treated with different concentrations of potassium iodide, and IL-1β, IL-18, lactate dehydrogenase (LDH), GSDMD were measured. Transcriptome chip analysis was used to explore the differentially expressed genes involved in pyroptosis of thyroid follicular cells induced by potassium iodide treatment.Results:The levels of IL-1β and IL-18 cytokines in the tissues of patients with Hashimoto′s thyroiditis and thyroid cancer were higher than control tissues ( P<0.01), and the activation of the pyroptosis executive protein GSDMD was significant increased, while GSDME was not activated. IL-1β, IL-18, and LDH secretion were significantly increased in response to potassium iodide stimulation in thyroid follicular cells ( P<0.01) and GSDMD was cleaved, which indicated that potassium iodide induced the pyroptosis of thyroid follicular cells. Moreover, potassium iodide could activate NLRP3 inflammasomes to promotethe pyroptosis of thyroid follicular cells. Transcriptome chip analysis further found that PARP1 protein was highly upregulated by the stimulation of potassium iodide, and then enhanced the activity of nuclear factor-κB (NF-κB) transcription factor to induce pyroptosis. Conclusions:The findings in this study reveal that potassium iodide promotesthe pyroptosis of thyroid follicular cells through activating NF-κB-NLRP3 inflammasome, which may be a novel mechanism that promots the development of Hashimoto′s thyroiditis under the condition of excessive iodine intake. PARP1 is a pivotal protein that mediates the pyroptosis induced by potassium iodide and may be a potential therapeutic target to control Hashimoto′s thyroiditis progression.
