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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.

Authors+Show Affiliations

Department of Pediatrics, Peking University First Hospital, Xi-An Men Street No. 1, West district, Beijing 100034, PR China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

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 -