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应激颗粒调控镉诱导的肺上皮细胞凋亡

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目的 探究应激颗粒调控环境金属镉暴露诱导肺上皮细胞凋亡的生物学功能.方法 将肺上皮细胞暴露于氯化镉,收集细胞进行PI/AnnexinV染色后使用流式细胞术检测氯化镉暴露后肺上皮细胞凋亡情况.通过免疫荧光实验检测应激颗粒的生成情况,Western Blot实验检测目的蛋白嘌呤霉素、真核翻译起始因子2亚基α(eukaryotic initiation factor 2α,eIF2α)、eIF2α磷酸化(p-eIF2α)的表达水平.结果 氯化镉暴露可以诱导肺上皮细胞发生凋亡.应激颗粒生成可抑制氯化镉诱导的肺上皮细胞凋亡.应激颗粒的形成伴随着eIF2α的磷酸化,抑制eIF2α磷酸化后应激颗粒生成减少.结论 eIF2α磷酸化介导的应激颗粒形成可以调控氯化镉暴露引起的肺上皮细胞凋亡.
Stress granules regulate cadmium-induced apoptosis of lung epithelial
Objective:This study aims to investigate the effect of stress granules(SGs)on cadmium-induced cell apoptosis in lung epithelial cells.Methods:Cadmium chloride-exposed lung epithelial cells were collected for PI/AnnexinV staining and then were detected by flow cytometry.Immunofluorescence assay was used to detect the formation of stress granules.Western blot assay was used to detect the expression level of Puromycin,eukaryotic translation initiation factor 2 subunit alpha(eIF2α)and phosphorylation of eIF2α(p-eIF2α).Results:Cadmium exposure can induce apoptosis of lung epithelial cells.Stress granules formation decreases cell apoptosis induced by cadmium exposure.The formation of stress granules is accompanied by phosphorylation of eIF2α.Inhibition of eIF2α phosphorylation inhibits the formation of stress granules.Conclusion:Phosphorylation of eIF2α-dependent stress granules could regulate cadmium-induced lung epithelial cell apoptosis.

stress granulescadmiumlung epithelial cellsapoptosis

张灿、张书平、张楠

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山东第一医科大学(山东省医学科学院)生物医学科学学院,山东 济南 250117

山东第一医科大学(山东省医学科学院)医学科技创新中心,山东 济南 250117

应激颗粒 肺上皮细胞 细胞凋亡

山东省泰山学者青年专家项目

tsqn202103105

2024

山东第一医科大学(山东省医学科学院)学报
泰山医学院

山东第一医科大学(山东省医学科学院)学报

影响因子:0.6
ISSN:2097-0005
年,卷(期):2024.45(8)