Abstract
S-sulfhydration is a signalling pathway of hydrogen sulfide (H2S), which is suggested as an anti-atherogenic molecule that may protect against atherosclerosis. The identification of S-sulfhydrated proteins by proteomic approach could be a major step towards understanding the mechanisms of H2S in response to atherosclerosis. The present study studied targeted S-sulfhydrated proteins using the modified biotin switch method followed by matrix-assisted laser desorption/ionisation time of flight tandem mass spectrometry identification. The results showed that H2S can protect against atherosclerosis by reducing body weight gain and alleviating aortic plaque formation. In addition, H2S treatment can increase aortic protein S-sulfhydration. Seventy targeted S-sulfhydrated aortic proteins were identified, mainly involved in metabolism, stimulus response and biological regulation, as determined by gene ontology database analysis. H2S also induced S-sulfhydration of glutathione peroxidase 1 and further reduced lipid peroxidation and increased antioxidant defence in the aorta by prompting glutathione synthesis. Our data suggest that H2S is a cardiovascular-protective molecule that S-sulfhydrates a subset of proteins that are mainly responsible for lipid metabolism and exerts its cytoprotective effects to clear free radicals and inhibit oxidative stress through cysteine S-sulfhydration.
Highlights
Hydrogen sulfide (H2S) is one of the three molecules most recently identified as gasotransmitters [1]
All apolipoprotein E knockout (ApoE KO) mice were first fed with an atherogenic diet for 4 weeks
The body weight gain in the H2S group was significantly reduced after H2S treatment, whereas the control group body weight remained similar over the whole period of treatment (Fig 1A)
Summary
Hydrogen sulfide (H2S) is one of the three molecules (along with nitric oxide and carbon monoxide) most recently identified as gasotransmitters [1]. Despite its toxicity, it is recognised as an endogenously produced gaseous signalling molecule that induces a variety of beneficial reactions in cardiovascular tissues [2]. Accumulating evidence suggests an association between atherosclerosis and deficiency in vascular cystathionine γ-lyase (CSE), an enzyme responsible for endogenous H2S production. It was shown by using CSE knockout mice that CSE gene deletion led to a decrease in H2S production with accelerated atherosclerosis [4]. The mechanism by which H2S reduces atherosclerosis is still not clear
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