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Cited by 307Sulfur Compounds in BiologyAtherosclerosis and Cardiovascular DiseasesNitric Oxide and Endothelin Effects

Role of Hydrogen Sulfide in the Development of Atherosclerotic Lesions in Apolipoprotein E Knockout Mice

Wang, Yanfei, Zhao, Xia, Jin, Hongfang, Wei, Hongling, Li, Wei, Bu, Dingfang, Tang, Xiuying, Ren, Yali +2 more·2009·Arteriosclerosis, Thrombosis, and Vascular Biology
DOI 10.1161/atvbaha.108.179333
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Abstract

Objective— We explored the effect of hydrogen sulfide (H 2 S) on atherosclerotic progression, particularly on intracellular adhesion molecule-1 (ICAM-1) in apolipoprotein-E knockout (apoE −/− ) mice and human umbilical vein endothelial cells (HUVECs). Methods and Results— ApoE −/− mice were treated with sodium hydrosulfide (NaHS) or DL-propargylglycine (PPG); HUVECs were pretreated with NaHS. Compared with control mice, apoE −/− mice showed decreased plasma H 2 S level and aortic H 2 S production but increased plasma ICAM-1 and aortic ICAM-1 protein and mRNA. Compared with apoE −/− mice, apoE −/− +NaHS mice showed increased plasma H 2 S level, but decreased size of atherosclerotic plaque and plasma and aortic ICAM-1 levels, whereas apoE −/− +PPG mice showed decreased plasma H 2 S level but enlarged plaque size and increased plasma and aortic ICAM-1 levels. NaHS suppressed ICAM-1 expression in tumor necrosis factor (TNF)-α–treated HUVECs. NaHS inhibited IκB degradation and NF-κB nuclear translocation in HUVECs treated with TNF-α. Conclusions— The vascular CSE/H 2 S pathway was disturbed in apoE −/− mice. H 2 S exerted an antiatherogenic effect and inhibited ICAM-1 expression in apoE −/− mice. H 2 S inhibited ICAM-1 expression in TNF-α-induced HUVECs via the NF-κB pathway.

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  • The H2S donor sodium hydrosulfide reduces atherosclerosis in Apoe-knockout mice, whereas genetic targeting of the H2S synthesizing enzyme cystathionine γ-lyase exacerbates atherosclerosis in this model.

    “The H2S donor sodium hydrosulfide reduces atherosclerosis in Apoe -knockout mice132, whereas genetic targeting of the H2S synthesizing enzyme cystathionine γ-lyase exacerbates atherosclerosis in this model98.”

    From Inflammation and its resolution in atherosclerosis: mediators and therapeutic opportunities (2019) · cites this paper as [132]

  • A decrease in H2S levels in atherosclerosis might lead to failure in resolution of atherosclerotic inflammation, raising the possibility that H2S donors could have a therapeutic role in cardiovascular disease prevention.

    “A decrease in H2S levels in atherosclerosis132 might, therefore, lead to a failure in the resolution of the atherosclerotic inflammation process, raising the possibility that H2S donors could have a therapeutic role in cardiovascular disease prevention.”

    From Inflammation and its resolution in atherosclerosis: mediators and therapeutic opportunities (2019) · cites this paper as [132]

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Research works printed but not linked: 2

  1. Ying L, Jie M, Junbao D, Yaguang D, Chaoshu T. Changes of a new gaseous signal molecule -hydrogen sulfide in children with hyperlipid- emia. J Appl Clin Pediatr. 2006;21:201-202.
  2. Elangbam CS, Qualls CW Jr, Dahlgren RR. Cell adhesion molecule- s-update. Vet Pathol. 1997;34:61-73.

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Authors
Wang, Y., Zhao, X., Jin, H., Wei, H., Li, W., Bu, D., Tang, X., Ren, Y., Tang, C., & Du, J.
Affiliations
  • Ministry of Education of the People's Republic of China (CN)
  • From the Department of Pediatrics (Y.W., X.Z., H.J., H.W., W.L., J.D.), Central Laboratory (D.B.), the Department of Electron Microscopy (X.T., Y.R.), and the Institute of Cardiovascular Research (C.T.), Peking University First Hospital, Beijing; and Key Laboratory of Molecular Cardiovascular Diseases (C.T., J.D.), Ministry of Education, Beijing, P.R. China.
ORCID
Venue
Arteriosclerosis, Thrombosis, and Vascular Biology
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2009-02
Volume
29
Issue
2
Pages
173-179
ISSN
  • 1079-5642 (ISSN-L)
  • 1524-4636
DOI
10.1161/atvbaha.108.179333
OpenAlex
W2110776535
Cited by
307
References
40
Citations by year
2026: 4 · 2025: 8 · 2024: 14 · 2023: 14 · 2022: 21 · 2021: 14 · 2020: 25 · 2019: 12 · 2018: 13 · 2017: 17 · 2016: 20 · 2015: 33 · 2014: 24 · 2013: 29 · 2012: 18
FWCI
6.38
Type
journal article
Language
en
Open access
closed
Locations
  • Arteriosclerosis Thrombosis and Vascular Biology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Natural Science Foundation of China (30571971, 30630031)
  • National Science Fund for Distinguished Young Scholars
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Sulfur Compounds in Biology
  • Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
  • Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
Keywords
hydrogen sulfide, atherosclerosis, ApoE-deficient mice, ICAM-1, endothelial cells, sodium hydrosulfide, DL-propargylglycine, cysteine sulfoxide reductase, NF-κB signaling, TNF-α, atherosclerotic plaque, antiatherogenic effects
MeSH terms
Alkynes, Animals, Aorta, Apolipoproteins E, Body Weight, Cardiovascular Agents, Cells, Cultured, Cystathionine gamma-Lyase, Disease Models, Animal, Dose-Response Relationship, Drug, Enzyme Inhibitors, Foam Cells, Glycine, Humans, Hydrogen Sulfide, Lipids, Male, Mice, Inbred C57BL, Muscle, Smooth, Vascular, RNA, Messenger, Sulfides, Tumor Necrosis Factor-alpha, NF-kappa B, Mice, Knockout, Intercellular Adhesion Molecule-1, I-kappa B Proteins, Active Transport, Cell Nucleus, Endothelial Cells, Atherosclerosis, Mice

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