Abstract
Hydrogen sulfide (H2S) is an endogenous signaling molecule which is important for cardiovascular health, but its mechanism of action remains poorly understood. Here, we report measurements of H2S as well as its oxidized metabolites, termed small oxoacids of sulfur (SOS = HSOH and HOSOH), in four human primary vascular cell lines: smooth muscle and endothelial cells derived from both human arterial and coronary tissues. We use a methodology that targets small molecular weight sulfur species; mass spectrometric analysis allows for species quantification to report cellular concentrations based on an H2S calibration curve. The production of H2S and SOS is orders of magnitude higher in smooth muscle (nanomolar) as compared to endothelial cell lines (picomolar). In all the primary lines measured, the distributions of these three species were HOSOH >H2S > HSOH, with much higher SOS than seen previously in non-vascular cell lines. H2S and SOS were effluxed from smooth muscle cells in higher concentrations than endothelial cells. Aortic smooth muscle cells were used to examine changes under hypoxic growth conditions. Hypoxia caused notable increases in HSOH and ROS, which we attribute to enhanced sulfide quinone oxidase activity that results in reverse electron transport.
Highlights
Like nitric oxide (NO) and carbon monoxide (CO), hydrogen sulfide (H2S) is a gasotransmitter that has been shown to be involved in many regulatory, cytoprotective, and signaling roles in human health, especially in cardiovascular diseases [1,2,3,4,5,6]
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Summary
Like nitric oxide (NO) and carbon monoxide (CO), hydrogen sulfide (H2S) is a gasotransmitter that has been shown to be involved in many regulatory, cytoprotective, and signaling roles in human health, especially in cardiovascular diseases [1,2,3,4,5,6]. CBS is important in producing H2S in the central nervous system [9], whereas CSE is thought to dominate H2S production in the cardiovasculature [10]; both enzymes are found concurrently expressed in many other tissues, e.g., the liver and kidney [11,12]. The activity of H2S and NO are entwined [15] It has been suggested H2S is predominately generated in vascular smooth muscle cells and nitric oxide in endothelial cells [16,17]. There is speculation that vasorelaxation and other cardiovascular effects are induced through biotransformation resulting in persulfide (e.g., RSSH) [24] or other modifications of protein thiols that can alter biochemical activity [25].
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