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氯化汞诱导的细胞凋亡与鸡胚肾细胞 PERK-ATF4-CHOP 通路的上调有关。

Apoptosis induced by mercuric chloride is associated with upregulation of PERK-ATF4-CHOP pathway in chicken embryonic kidney cells.

机构信息

College of Animal Science and Technology, Henan University of Science and Technology, Luoyang, China.

College of Animal Science and Technology, Henan University of Science and Technology, Luoyang, China.

出版信息

Poult Sci. 2020 Nov;99(11):5802-5813. doi: 10.1016/j.psj.2020.06.084. Epub 2020 Aug 12.

Abstract

Mercuric chloride (HgCl) is a serious environmental toxicant. So far, the toxicity mechanism of HgCl in chicken embryonic kidney (CEK) cells is not still fully understood. In this study, the possible molecular mechanisms of HgCl on apoptosis of CEK cells were investigated. Results showed that the cell morphology changed, and cell viability was significantly decreased (P < 0.05) after HgCl exposure. Besides, apoptosis rate was significantly increased after HgCl exposure (P < 0.05). The gene and protein expressions of B-cell lymphoma-2 associate X/B-cell lymphoma-2 (P < 0.05), caspase-3 (P < 0.05), and caspase-9 (P < 0.05) were significantly enhanced by HgCl in CEK cells. We also found that intracellular reactive oxygen species level was significantly enhanced (P < 0.05), and the flux of calcium ion to mitochondria occurred after HgCl exposure. In terms of molecular mechanisms, the mRNA and protein expressions associated with endoplasmic reticulum (ER) stress were significantly increased after HgCl exposure (P < 0.05), including glucose regulated protein 78, protein kinase RNA-like endoplasmic reticulum kinase (PERK), activating transcription factor 4 (ATF4), and C/EBP homologous protein (CHOP). However, pretreated with 1-μmol/L 4-phenylbutyrate (ER stress inhibitor) alleviated the apoptosis and downregulated PERK-ATF4-CHOP pathway in CEK cells. Taken together, upregulation of PERK-ATF4-CHOP pathway of ER stress induced by HgCl is associated with apoptosis in CEK cells.

摘要

氯化汞(HgCl)是一种严重的环境毒物。迄今为止,HgCl 对鸡胚肾(CEK)细胞毒性的作用机制尚未完全阐明。本研究旨在探讨 HgCl 诱导 CEK 细胞凋亡的可能分子机制。结果表明,HgCl 暴露后细胞形态发生改变,细胞活力显著降低(P<0.05)。此外,HgCl 暴露后细胞凋亡率显著增加(P<0.05)。HgCl 可显著上调 CEK 细胞中 B 细胞淋巴瘤-2 相关 X/B 细胞淋巴瘤-2(P<0.05)、半胱氨酸天冬氨酸蛋白酶-3(caspase-3)(P<0.05)和半胱氨酸天冬氨酸蛋白酶-9(caspase-9)(P<0.05)的基因和蛋白表达。我们还发现,HgCl 暴露后细胞内活性氧水平显著升高(P<0.05),钙离子流向线粒体。从分子机制上看,HgCl 暴露后与内质网(ER)应激相关的 mRNA 和蛋白表达显著增加(P<0.05),包括葡萄糖调节蛋白 78、蛋白激酶 RNA 样内质网激酶(PERK)、激活转录因子 4(ATF4)和 C/EBP 同源蛋白(CHOP)。然而,用 1μmol/L 4- 苯基丁酸(ER 应激抑制剂)预处理可减轻 CEK 细胞凋亡,并下调 PERK-ATF4-CHOP 通路。综上所述,HgCl 诱导的 ER 应激 PERK-ATF4-CHOP 通路的上调与 CEK 细胞凋亡有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8226/7647797/ed64b400e786/gr1.jpg

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