Sulfhydrated Sirtuin-1 Increasing Its Deacetylation Activity Is an Essential Epigenetics Mechanism of Anti-Atherogenesis by Hydrogen Sulfide

Hydrogen sulfide (H2S) has a protective role in the pathogenesis of atherosclerosis by multiple pathways. Sirtuin-1 ( ) is a histone deacetylase, as an essential mediated longevity gene, and has an anti-atherogenic effect by regulating the acetylation of some functional proteins. Whether is involved...

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Vydané v:	Antioxidants & redox signaling Ročník 30; číslo 2; s. 184
Hlavní autori:	Du, Congkuo, Lin, Xianjuan, Xu, Wenjing, Zheng, Fengjiao, Cai, Junyan, Yang, Jichun, Cui, Qinghua, Tang, Chaoshu, Cai, Jun, Xu, Guoheng, Geng, Bin
Médium:	Journal Article
Jazyk:	English
Vydavateľské údaje:	United States 10.01.2019
Predmet:	Acetylation Animals Apolipoproteins E - deficiency Atherosclerosis - drug therapy Atherosclerosis - etiology Atherosclerosis - metabolism Atherosclerosis - pathology Biomarkers Cell Line Cholesterol - metabolism Disease Models, Animal Endothelium - metabolism Epigenesis, Genetic Foam Cells - metabolism Foam Cells - pathology Gene Expression Humans Hydrogen Sulfide - pharmacology Immunohistochemistry Mice Mice, Knockout Plaque, Atherosclerotic - drug therapy Plaque, Atherosclerotic - etiology Plaque, Atherosclerotic - metabolism Plaque, Atherosclerotic - pathology Protein Processing, Post-Translational Sirtuin 1 - genetics Sirtuin 1 - metabolism Ubiquitination atherosclerosis sirtuin1 sulfhydration hydrogen sulfide cystathionine gamma lyase
ISSN:	1557-7716, 1557-7716
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Shrnutí:	Hydrogen sulfide (H2S) has a protective role in the pathogenesis of atherosclerosis by multiple pathways. Sirtuin-1 ( ) is a histone deacetylase, as an essential mediated longevity gene, and has an anti-atherogenic effect by regulating the acetylation of some functional proteins. Whether is involved in protecting H2S in atherosclerosis and its mechanism remains unclear. In ApoE-knockout atherosclerosis mice, treatment with an H2S donor (NaHS or GYY4137) reduced atherosclerotic plaque area, macrophage infiltration, aortic inflammation, and plasma lipid level. H2S treatment increased aorta and liver mRNA expression. Overexpression or slicing cystathionine gamma lyase (CSE) also changed intracellular expression. CSE/H2S treatment increased deacetylation in endothelium and hepatocytes and macrophages, then induced deacetylation of its target proteins (P53, P65, and sterol response element binding protein), thereby reducing endothelial and macrophage inflammation and inhibiting macrophage cholesterol uptake and cholesterol synthesis of liver. Also, CSE/H2S induced sulfhydration at its two zinc finger domains, increased its zinc ion binding activity to stabilize the alpha-helix structure, lowered its ubiquitination, and reduced its degradation. H2S is a novel activator by direct sulfhydration. Because has a role in longevity, H2S may be a protector for aging-related diseases. Endogenous CSE/H2S directly sulfhydrated , enhanced binding to zinc ion, then promoted its deacetylation activity, and increased stability, thus reducing atherosclerotic plaque formation.
Bibliografia:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	1557-7716 1557-7716
DOI:	10.1089/ars.2017.7195