on November 6, 2008
Published online before print November 6, 2008, doi: 10.1161/ATVBAHA.108.179333
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Submitted on December 24, 2007
Accepted on October 29, 2008
Role of Hydrogen Sulfide in the Development of Atherosclerotic Lesions in Apolipoprotein E Knockout Mice
Yanfei Wang ;
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.
* To whom correspondence should be addressed. 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, 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 I
B degradation and NFB 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 NFB pathway.
Key words: hydrogen sulfide • intercellular adhesion molecule-1 • atherosclerosis • apolipoprotein E knockout mice • human umbilical vein endothelial cells
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