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Role of hydrogen sulfide in the development of atherosclerotic lesions in apolipoprotein E knockout mice.
Arterioscler Thromb Vasc Biol. 2009 Feb; 29(2):173-9.AT

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)-alpha-treated HUVECs. NaHS inhibited IkappaB degradation and NF-kappaB nuclear translocation in HUVECs treated with TNF-alpha.

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-alpha-induced HUVECs via the NF-kappaB pathway.

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Authors+Show Affiliations

Wang Y
Department of Pediatrics, Peking University First Hospital, Xi-An Men Street No. 1, West district, Beijing 100034, PR China.
Zhao X
No affiliation info available
Jin H
No affiliation info available
Wei H
No affiliation info available
Li W
No affiliation info available
Bu D
No affiliation info available
Tang X
No affiliation info available
Ren Y
No affiliation info available
Tang C
No affiliation info available
Du J
No affiliation info available

MeSH

Active Transport, Cell NucleusAlkynesAnimalsAortaApolipoproteins EAtherosclerosisBody WeightCardiovascular AgentsCells, CulturedCystathionine gamma-LyaseDisease Models, AnimalDose-Response Relationship, DrugEndothelial CellsEnzyme InhibitorsFoam CellsGlycineHumansHydrogen SulfideI-kappa B ProteinsIntercellular Adhesion Molecule-1LipidsMaleMiceMice, Inbred C57BLMice, KnockoutMuscle, Smooth, VascularNF-kappa BRNA, MessengerSulfidesTumor Necrosis Factor-alpha

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18988885

Citation

Wang, Yanfei, et al. "Role of Hydrogen Sulfide in the Development of Atherosclerotic Lesions in Apolipoprotein E Knockout Mice." Arteriosclerosis, Thrombosis, and Vascular Biology, vol. 29, no. 2, 2009, pp. 173-9.
Wang Y, Zhao X, Jin H, et al. Role of hydrogen sulfide in the development of atherosclerotic lesions in apolipoprotein E knockout mice. Arterioscler Thromb Vasc Biol. 2009;29(2):173-9.
Wang, Y., Zhao, X., Jin, H., Wei, H., Li, W., Bu, D., Tang, X., Ren, Y., Tang, C., & Du, J. (2009). Role of hydrogen sulfide in the development of atherosclerotic lesions in apolipoprotein E knockout mice. Arteriosclerosis, Thrombosis, and Vascular Biology, 29(2), 173-9. https://doi.org/10.1161/ATVBAHA.108.179333
Wang Y, et al. Role of Hydrogen Sulfide in the Development of Atherosclerotic Lesions in Apolipoprotein E Knockout Mice. Arterioscler Thromb Vasc Biol. 2009;29(2):173-9. PubMed PMID: 18988885.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Role of hydrogen sulfide in the development of atherosclerotic lesions in apolipoprotein E knockout mice. AU - Wang,Yanfei, AU - Zhao,Xia, AU - Jin,Hongfang, AU - Wei,Hongling, AU - Li,Wei, AU - Bu,Dingfang, AU - Tang,Xiuying, AU - Ren,Yali, AU - Tang,Chaoshu, AU - Du,Junbao, Y1 - 2008/11/06/ PY - 2008/11/8/pubmed PY - 2009/2/6/medline PY - 2008/11/8/entrez SP - 173 EP - 9 JF - Arteriosclerosis, thrombosis, and vascular biology JO - Arterioscler Thromb Vasc Biol VL - 29 IS - 2 N2 - 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)-alpha-treated HUVECs. NaHS inhibited IkappaB degradation and NF-kappaB nuclear translocation in HUVECs treated with TNF-alpha. 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-alpha-induced HUVECs via the NF-kappaB pathway. SN - 1524-4636 UR - https://www.unboundmedicine.com/medline/citation/18988885/Role_of_hydrogen_sulfide_in_the_development_of_atherosclerotic_lesions_in_apolipoprotein_E_knockout_mice_ L2 - https://www.ahajournals.org/doi/10.1161/ATVBAHA.108.179333?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -