Role of PERK-Mediated Endoplasmic Reticulum Stress in Ferroptosis Caused by Hexavalent Chromium in Chicken Hepatocytes

被引：2

作者：

Cui, Yukun ^{[1
]}

Zhang, Pu ^{[3
]}

Song, Kaimin ^{[1
]}

Qi, Changxi ^{[1
]}

Liu, Yongxia ^{[2
]}

Liu, Jianzhu ^{[1
]}

机构：

[1] Shandong Agr Univ, Coll Vet Med, Tai An 271018, Shandong, Peoples R China

[2] Shandong Agr Univ, Res Ctr Anim Dis Control Engn, Tai An 271018, Shandong, Peoples R China

[3] Qingdao Univ, Affiliated Taian City Cent Hosp, Tai An 271000, Shandong, Peoples R China

来源：

BIOLOGICAL TRACE ELEMENT RESEARCH | 2024年 / 202卷 / 11期

基金：

中国国家自然科学基金;

关键词：

Cr(VI); Chicken hepatocytes; Ferroptosis; Endoplasmic reticulum stress; PERK; LIPID-PEROXIDATION; CELL-DEATH;

D O I：

10.1007/s12011-023-04046-8

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

This study aimed to investigate whether Cr(VI) can induce ferroptosis in chicken hepatocytes and determine the role of PERK-mediated endoplasmic reticulum stress (ERS). First, a model of Cr(VI) poisoning was established by exposing chicken hepatocytes to Cr(VI). The levels of ferroptosis-related proteins, meanwhile, GSH, SOD, MDA, and lipid ROS, were measured. Furthermore, the expression of GRP78 and PERK proteins was examined. Changes in ERS and ferroptosis were evaluated by silencing the PERK gene. Results showed that Cr(VI) led to the accumulation of lipid ROS, decreased expression of GPX4 and HSP27, increased expression of COX2, and induced ferroptosis in chicken hepatocytes. Exposure to Cr(VI) increased the protein expression of GRP78 and PERK, and silencing of PERK worsened Cr(VI)-induced ferroptosis. In conclusion, Cr(VI) can induce ferroptosis in chicken hepatocytes, and PERK plays an important role as a negative regulator.

引用

页码：5208 / 5218

页数：11

共 43 条

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