CLC number:
On-line Access: 2023-05-15
Received: 2022-12-29
Revision Accepted: 2023-01-27
Crosschecked: 2023-05-16
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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.
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