PMID- 37422542
OWN - NLM
STAT- MEDLINE
DCOM- 20240221
LR  - 20240221
IS  - 1559-0720 (Electronic)
IS  - 0163-4984 (Linking)
VI  - 202
IP  - 4
DP  - 2024 Apr
TI  - Bisphenol A Regulates the TNFR1 Pathway and Excessive ROS Mediated by 
      miR-26a-5p/ADAM17 Axis to Aggravate Selenium Deficiency-Induced Necroptosis in 
      Broiler Veins.
PG  - 1722-1740
LID - 10.1007/s12011-023-03756-3 [doi]
AB  - Selenium (Se) deficiency can affect the expression of microRNA (miRNA) and induce 
      necroptosis, apoptosis, etc., resulting in damage to various tissues and organs. 
      Bisphenol A (BPA) exposure can cause adverse consequences such as oxidative 
      stress, endothelial dysfunction, and atherosclerosis. The toxic effects of 
      combined treatment with Se-deficiency and BPA exposure may have a synergistic 
      effect. We replicated the BPA exposure and Se-deficiency model in broiler to 
      investigate whether the combined treatment of Se-deficiency and BPA exposure 
      induced necroptosis and inflammation of chicken vascular tissue via the 
      miR-26A-5p/ADAM17 axis. We found that Se deficiency and BPA exposure 
      significantly inhibited the expression of miR-26a-5p and increased the expression 
      of ADAM17, thereby increasing reactive oxygen species (ROS) production. 
      Subsequently, we discovered that the tumor necrosis factor receptor (TNFR1), 
      which was highly expressed, activated the necroptosis pathway through 
      receptor-interacting protein kinase 1 (RIPK1), receptor-interacting protein 
      kinase 3 (RIPK3), and mixed-lineage kinase domain-like (MLKL), and regulated the 
      heat shock proteins-related genes expressions and inflammation-related genes 
      expressions after exposure to BPA and selenium deficiency. In vitro, we found 
      that miR-26a-5p knockdown and increased ADAM17 can induce necroptosis by 
      activating the TNFR1 pathway. Similarly, both N-Acetyl-L-cysteine (NAC), 
      Necrostatin-1 (Nec-1), and miR-26a-5p mimic prevented necroptosis and 
      inflammation caused by BPA exposure and Se deficiency. These results suggest that 
      BPA exposure activates the miR-26a-5p/ADAM17 axis and exacerbates Se 
      deficient-induced necroptosis and inflammation through the TNFR1 pathway and 
      excess ROS. This study lays a data foundation for future ecological and health 
      risk assessments of nutrient deficiencies and environmental toxic pollution.
CI  - (c) 2023. The Author(s), under exclusive licence to Springer Science+Business 
      Media, LLC, part of Springer Nature.
FAU - Fan, Xue
AU  - Fan X
AD  - College of Veterinary Medicine, Northeast Agricultural University, Harbin, 
      150030, People's Republic of China.
FAU - Wang, Yixuan
AU  - Wang Y
AD  - College of Veterinary Medicine, Northeast Agricultural University, Harbin, 
      150030, People's Republic of China.
FAU - Zhang, Jintao
AU  - Zhang J
AD  - College of Veterinary Medicine, Northeast Agricultural University, Harbin, 
      150030, People's Republic of China.
FAU - Lin, Hongjin
AU  - Lin H
AD  - College of Veterinary Medicine, Northeast Agricultural University, Harbin, 
      150030, People's Republic of China.
FAU - Bai, Zhikun
AU  - Bai Z
AD  - School of Basic Medical Sciences, Youjiang Medical University for Nationalities, 
      Baise, 533000, China. lishu@neau.edu.cn.
FAU - Li, Shu
AU  - Li S
AD  - College of Veterinary Medicine, Northeast Agricultural University, Harbin, 
      150030, People's Republic of China. bai.zhikun@ymun.edu.cn.
LA  - eng
GR  - ZD2022C005/Natural Science Foundation of Heilongjiang Province/
GR  - No. 32072811/National Natural Science Foundation of China/
PT  - Journal Article
DEP - 20230708
PL  - United States
TA  - Biol Trace Elem Res
JT  - Biological trace element research
JID - 7911509
RN  - 0 (Benzhydryl Compounds)
RN  - MLT3645I99 (bisphenol A)
RN  - 0 (MicroRNAs)
RN  - 0 (Phenols)
RN  - EC 2.7.- (Protein Kinases)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Receptors, Tumor Necrosis Factor)
RN  - 0 (Receptors, Tumor Necrosis Factor, Type I)
RN  - H6241UJ22B (Selenium)
SB  - IM
MH  - Animals
MH  - Apoptosis
MH  - *Benzhydryl Compounds
MH  - Chickens/metabolism
MH  - Inflammation/chemically induced
MH  - *MicroRNAs/genetics/metabolism
MH  - Necroptosis
MH  - *Phenols
MH  - Protein Kinases/metabolism
MH  - Reactive Oxygen Species/metabolism
MH  - Receptors, Tumor Necrosis Factor
MH  - Receptors, Tumor Necrosis Factor, Type I/metabolism
MH  - *Selenium/metabolism
OTO - NOTNLM
OT  - ADAM17
OT  - Bisphenol A
OT  - Necroptosis
OT  - Selenium deficiency
OT  - Vein
OT  - miR-26a-3p
EDAT- 2023/07/09 01:07
MHDA- 2024/02/12 15:42
CRDT- 2023/07/08 23:20
PHST- 2023/05/25 00:00 [received]
PHST- 2023/06/28 00:00 [accepted]
PHST- 2024/02/12 15:42 [medline]
PHST- 2023/07/09 01:07 [pubmed]
PHST- 2023/07/08 23:20 [entrez]
AID - 10.1007/s12011-023-03756-3 [pii]
AID - 10.1007/s12011-023-03756-3 [doi]
PST - ppublish
SO  - Biol Trace Elem Res. 2024 Apr;202(4):1722-1740. doi: 10.1007/s12011-023-03756-3. 
      Epub 2023 Jul 8.