Integrated proteomic analysis to explore the molecular regulation mechanism of IL‐33 mRNA increased by black carbon in the human endothelial cell line EA.hy926. Issue 10 (1st July 2022)
- Record Type:
- Journal Article
- Title:
- Integrated proteomic analysis to explore the molecular regulation mechanism of IL‐33 mRNA increased by black carbon in the human endothelial cell line EA.hy926. Issue 10 (1st July 2022)
- Main Title:
- Integrated proteomic analysis to explore the molecular regulation mechanism of IL‐33 mRNA increased by black carbon in the human endothelial cell line EA.hy926
- Authors:
- Jiang, Wanyu
Chu, Hongqian
Li, Zekang
Ge, Jianhong
Wang, Xiaoyun
Jiang, Jianjun
Xiao, Qianqian
Meng, Qinghe
Lou, Yaxin
Hao, Weidong
Wei, Xuetao - Abstract:
- Abstract: Black carbon (BC) correlates with the occurrence and progression of atherosclerosis and other cardiovascular diseases. Increasing evidence has demonstrated that BC could impair vascular endothelial cells, but the underlying mechanisms remain obscure. It is known that IL‐33 exerts a significant biological role in cardiovascular disease, but little is known about the molecular regulation of IL‐33 expression at present. We first found that BC significantly increased IL‐33 mRNA in EA.hy926 cells in a concentration and time‐dependent manner, and we conducted this study to explore its underlying mechanism. We identified that BC induced mitochondrial damage and suppressed autophagy function in EA.hy926 cells, as evidenced by elevation of the aspartate aminotransferase ( GOT2 ), reactive oxygen species (ROS) and p62, and the reduction of mitochondrial membrane potential (ΔΨm ). However, ROS cannot induce IL‐33 mRNA‐production in BC‐exposed EA.hy926 cells. Further, experiments revealed that BC could promote IL‐33 mRNA production through the PI3K/Akt/AP‐1 and p38/AP‐1 signaling pathways. It is concluded that BC could induce oxidative stress and suppress autophagy function in endothelial cells. This study also provided evidence that the pro‐cardiovascular‐diseases properties of BC may be due to its ability to stimulate the PI3K/AKT/AP‐1 and p38/AP‐1 pathway, further activate IL‐33 and ultimately result in a local vascular inflammation.
- Is Part Of:
- Environmental toxicology. Volume 37:Issue 10(2022)
- Journal:
- Environmental toxicology
- Issue:
- Volume 37:Issue 10(2022)
- Issue Display:
- Volume 37, Issue 10 (2022)
- Year:
- 2022
- Volume:
- 37
- Issue:
- 10
- Issue Sort Value:
- 2022-0037-0010-0000
- Page Start:
- 2434
- Page End:
- 2444
- Publication Date:
- 2022-07-01
- Subjects:
- black carbon -- EA.hy926 cells -- IL‐33 -- mitochondrial damage -- PI3K/Akt/AP‐1 and p38/AP‐1 pathways
Water quality bioassay -- Periodicals
Water -- Pollution -- Toxicology -- Periodicals
Microbiological assay -- Periodicals
Toxicity testing -- Periodicals
Environmental toxicology -- Periodicals
Environmental Pollution -- Periodicals
Environmental Pollutants -- Periodicals
Environmental Monitoring -- Periodicals
Écotoxicologie -- Périodiques
Pollution -- Périodiques
615.902 - Journal URLs:
- http://onlinelibrary.wiley.com/journal/10.1002/(ISSN)1522-7278 ↗
http://onlinelibrary.wiley.com/ ↗ - DOI:
- 10.1002/tox.23608 ↗
- Languages:
- English
- ISSNs:
- 1520-4081
- Deposit Type:
- Legaldeposit
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- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 3791.784000
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British Library HMNTS - ELD Digital store - Ingest File:
- 23404.xml