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Journal of Zhejiang University SCIENCE B 2023 Vol.24 No.5 P.406-417

http://doi.org/10.1631/jzus.B2200694


Role of selenoprotein M knockdown in the melatonin antagonism of nickel-induced apoptosis and endoplasmic reticulum stress in mouse heart


Author(s):  Xintong ZHANG, Xiaoxue GAI, Lihua XU, Wenxue MA, Qiaohan LIU, Bendong SHI, Cheng FANG, Jingzeng CAI, Ziwei ZHANG

Affiliation(s):  College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China; more

Corresponding email(s):   zhangziwei@neau.edu.cn, caijingzeng@neau.edu.cn

Key Words:  Selenoprotein M (SelM), Nickel chloride (NiCl2), Melatonin, Apoptosis, Mouse heart


Xintong ZHANG, Xiaoxue GAI, Lihua XU, Wenxue MA, Qiaohan LIU, Bendong SHI, Cheng FANG, Jingzeng CAI, Ziwei ZHANG. Role of selenoprotein M knockdown in the melatonin antagonism of nickel-induced apoptosis and endoplasmic reticulum stress in mouse heart[J]. Journal of Zhejiang University Science B, 2023, 24(5): 406-417.

@article{title="Role of selenoprotein M knockdown in the melatonin antagonism of nickel-induced apoptosis and endoplasmic reticulum stress in mouse heart",
author="Xintong ZHANG, Xiaoxue GAI, Lihua XU, Wenxue MA, Qiaohan LIU, Bendong SHI, Cheng FANG, Jingzeng CAI, Ziwei ZHANG",
journal="Journal of Zhejiang University Science B",
volume="24",
number="5",
pages="406-417",
year="2023",
publisher="Zhejiang University Press & Springer",
doi="10.1631/jzus.B2200694"
}

%0 Journal Article
%T Role of selenoprotein M knockdown in the melatonin antagonism of nickel-induced apoptosis and endoplasmic reticulum stress in mouse heart
%A Xintong ZHANG
%A Xiaoxue GAI
%A Lihua XU
%A Wenxue MA
%A Qiaohan LIU
%A Bendong SHI
%A Cheng FANG
%A Jingzeng CAI
%A Ziwei ZHANG
%J Journal of Zhejiang University SCIENCE B
%V 24
%N 5
%P 406-417
%@ 1673-1581
%D 2023
%I Zhejiang University Press & Springer
%DOI 10.1631/jzus.B2200694

TY - JOUR
T1 - Role of selenoprotein M knockdown in the melatonin antagonism of nickel-induced apoptosis and endoplasmic reticulum stress in mouse heart
A1 - Xintong ZHANG
A1 - Xiaoxue GAI
A1 - Lihua XU
A1 - Wenxue MA
A1 - Qiaohan LIU
A1 - Bendong SHI
A1 - Cheng FANG
A1 - Jingzeng CAI
A1 - Ziwei ZHANG
J0 - Journal of Zhejiang University Science B
VL - 24
IS - 5
SP - 406
EP - 417
%@ 1673-1581
Y1 - 2023
PB - Zhejiang University Press & Springer
ER -
DOI - 10.1631/jzus.B2200694


Abstract: 
The aim of this study was to investigate the role of selenoprotein M (SelM) in endoplasmic reticulum stress and apoptosis in nickel-exposed mouse hearts and to explore the detoxifying effects of melatonin. At 21 d after intraperitoneal injection of nickel chloride (NiCl2) and/or melatonin into male wild-type (WT) and SelM knockout (KO) C57BL/6J mice, NiCl2 was found to induce changes in the microstructure and ultrastructure of the hearts of both WT and SelM KO mice, which were caused by oxidative stress, endoplasmic reticulum stress, and apoptosis, as evidenced by decreases in malondialdehyde (MDA) content and total antioxidant capacity (T-AOC) activity. Changes in the messenger RNA (mRNA) and protein expression of genes related to endoplasmic reticulum stress (activating transcription factor 4 (ATF4), inositol-requiring protein 1 (IRE1), c-Jun N-terminal kinase (JNK), and C/EBP homologous protein (CHOP)) and apoptosis (B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein (Bax), Caspase-3, Caspase-9, and Caspase-12) were also observed. Notably, the observed damage was worse in SelM KO mice. Furthermore, melatonin alleviated the heart injury caused by NiCl2 in WT mice but could not exert a good protective effect in the heart of SelM KO mice. Overall, the findings suggested that the antioxidant capacity of SelM, as well as its modulation of endoplasmic reticulum stress and apoptosis, plays important roles in nickel-induced heart injury.

硒蛋白M敲除在褪黑素拮抗镍诱导的小鼠心脏细胞凋亡和内质网应激中的作用

张鑫彤1,盖晓雪2,徐礼华1,马文雪1,柳俏寒1,史本栋1,方程1,蔡敬增1,张子威1,3
1东北农业大学动物医学学院,中国哈尔滨市,150030
2绥化市农业农村局,中国绥化市,152000
3东北农业大学黑龙江省教育厅动物常见病防治重点实验室,中国哈尔滨市,150030
摘要:本研究旨在研究硒蛋白M(SelM)在由镍诱导的小鼠心脏内质网应激和细胞凋亡中的作用,并探索褪黑素的解毒作用。在对雄性野生型(WT)和SelM敲除型(KO)C57BL/6J小鼠腹腔注射氯化镍(NiCl2)和/或褪黑素21天后,我们发现NiCl2能诱发WT和SelM KO小鼠心脏的微观结构和超微结构的变化,并通过丙二醛(MDA)含量和总抗氧化能力(T-AOC)下降证明这些变化是由氧化应激、内质网应激和细胞凋亡引起的。同时,我们观察到与内质网应激(激活转录因子4(ATF4)、肌醇需要酶1(IRE1)、c-Jun N-端激酶(JNK)和C/EBP同源蛋白(CHOP))和细胞凋亡(B细胞淋巴瘤2型蛋白(Bcl-2)、Bcl-2相关蛋白X(Bax)、半胱氨酸-天冬氨酸蛋白酶3(Caspase-3)、Caspase-9和Caspase-12)相关基因的信使RNA(mRNA)和蛋白表达的变化。值得注意的是,这种损伤在SelM KO小鼠中更严重。此外,褪黑素减轻了WT小鼠由NiCl2引起的心脏损伤,但对SelM KO小鼠的心脏却不能产生良好的保护作用。综上所述,本研究结果表明SelM的抗氧化能力以及它对内质网应激和细胞凋亡的调节在镍引起的心脏损伤中起着重要作用。

关键词:硒蛋白M(SelM);氯化镍;褪黑素;细胞凋亡;小鼠心脏

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