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Title of Journal: Inflamm Res

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Abbravation: Inflammation Research

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Springer Basel

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DOI

10.1007/bf00178637

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1420-908X

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Association of hydrogen sulfide with alterations o

Authors: Lin Gao Zuojun Xu Zhaofang Yin Kan Chen Changqian Wang Huili Zhang
Publish Date: 2015/06/30
Volume: 64, Issue: 8, Pages: 627-635
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Abstract

Recent data in human and mice suggest that monocyte chemokine receptors CX3CR1 and CCR2 are involved in the pathogenesis of atherosclerosis Our previous study showed that hydrogen sulfide a novel gaseous mediator hampered the progression of atherosclerosis in fatfed apoE−/− mice with downregulating CX3CR1 and CX3CL1 expressions However there is a paucity of information regarding the clinical association between endogenous H2S metabolism and alterations of monocyte chemokine receptors in patients with cardiovascular disease Therefore in this study we investigated circulating monocyte heterogeneity with differential expressions of CCR2 and CX3CR1 and its relevance to plasma H2S level in patients with coronary artery disease CADSixtythree CAD patients with acute coronary syndrome ACS n = 46 or stable angina pectoris SAP n = 17 undergoing either percutaneous coronary intervention or coronary angiography and eleven nonCAD patients were enrolled in the study Plasma levels of H2S as well as chemokines CCL2 and CX3CL1 and expressions of CCR2 and CX3CR1 on peripheral monocytes were measuredIt was found that plasma H2S level was significantly reduced whereas plasma CCL2 and CX3CL1 levels were substantially elevated in patients with ACS as compared with patients with SAP or nonCAD patients Furthermore patients with ACS had significantly higher proportion of CD14+CCR2+CX3CR1+ and CD14+CCR2−CX3CR1+ monocytes but lower percentage of CD14+CCR2+CX3CR1− monocytes than SAP or nonCAD patients did Lastly plasma H2S level showed a significantly negative correlation with the proportion of CD14+CCR2+CX3CR1+ monocytes but not other monocyte subsetsThese data indicate that decreased endogenous H2S production may predispose stable CAD patients to rupture of vulnerable plaque and thus to ACS probably in relation to circulating monocyte phenotypic transformation with differential expressions of CCR2 and CX3CR1

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