This Article Full Text Full Text (PDF) Data Supplement All Versions of this Article: 29/2/173    most recent ATVBAHA.108.179333v1 Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Wang, Y. Articles by Du, J. Search for Related Content PubMed PubMed Citation Articles by Wang, Y. Articles by Du, J. Related Collections Genetically altered mice Growth factors/cytokines Mechanism of atherosclerosis/growth factors Related Article

(Arteriosclerosis, Thrombosis, and Vascular Biology. 2009;29:173.)
© 2009 American Heart Association, Inc.

Integrative Physiology/Experimental Medicine

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

Yanfei Wang; Xia Zhao; Hongfang Jin; Hongling Wei; Wei Li; Dingfang Bu; Xiuying Tang; Yali Ren; Chaoshu Tang; Junbao Du

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.

Correspondence to Junbao Du, MD, PhD, Department of Pediatrics, Peking University First Hospital, Xi-An Men Street No. 1, West district, Beijing 100034, P.R. China. E-mail junbaodu{at}ht.rol.cn.net

Objective— We explored the effect of hydrogen sulfide (H₂S) 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 H₂S level and aortic H₂S production but increased plasma ICAM-1 and aortic ICAM-1 protein and mRNA. Compared with apoE^–/– mice, apoE^–/–+NaHS mice showed increased plasma H₂S level, but decreased size of atherosclerotic plaque and plasma and aortic ICAM-1 levels, whereas apoE^–/–+PPG mice showed decreased plasma H₂S level but enlarged plaque size and increased plasma and aortic ICAM-1 levels. NaHS suppressed ICAM-1 expression in tumor necrosis factor (TNF)-–treated HUVECs. NaHS inhibited IB degradation and NF-B nuclear translocation in HUVECs treated with TNF-.

Conclusions— The vascular CSE/H₂S pathway was disturbed in apoE^–/– mice. H₂S exerted an antiatherogenic effect and inhibited ICAM-1 expression in apoE^–/– mice. H₂S inhibited ICAM-1 expression in TNF--induced HUVECs via the NF-B pathway.

Key Words: hydrogen sulfide • intercellular adhesion molecule-1 • atherosclerosis • apolipoprotein E knockout mice • human umbilical vein endothelial cells

Related Article:

Is H₂S a Stinky Remedy for Atherosclerosis?

Rui Wang
Arterioscler Thromb Vasc Biol 2009 29: 156-157. [Extract] [Full Text] [PDF]

This article has been cited by other articles:

				C. Zoccali, C. Catalano, and S. Rastelli Blood pressure control: hydrogen sulfide, a new gasotransmitter, takes stage Nephrol. Dial. Transplant., May 1, 2009; 24(5): 1394 - 1396. [Full Text] [PDF]

				R. Wang Is H2S a Stinky Remedy for Atherosclerosis? Arterioscler Thromb Vasc Biol, February 1, 2009; 29(2): 156 - 157. [Full Text] [PDF]