Histone acetylation and methylation significantly change with severity of atherosclerosis in human carotid plaques

Greißel, Anna; Culmes, Mihaela; Burgkart, Rainer; Zimmermann, Alexander; Eckstein, Hans‐Henning; Zernecke, Alma; Pelisek, Jaroslav

doi:10.1016/j.carpath.2015.11.001

Cited by 103 publications

(95 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The incidence and development of cardiovascular diseases are associated with acetylation of histone H3 at lysine 9 (H3K9ac), which is one of the most common histone acetylation forms. Compared to healthy vessels, increased histone acetylation at H3K9 was observed in smooth muscle cells (SMCs) in advanced atherosclerotic lesions and H3K9 acetylation in SMCs and macrophages correlates with plaque severity of atherosclerosis [Greissel et al, ]. HDAC1 can regulate most of the observed changes in histone acetylation, especially the acetylation of H3K9 [Loponte et al, ].…”

mentioning

confidence: 99%

miR‐34a Targets HDAC1‐Regulated H3K9 Acetylation on Lipid Accumulation Induced by Homocysteine in Foam Cells

Zhao

et al. 2017

J of Cellular Biochemistry

View full text Add to dashboard Cite

Hyperhomocysteinemia (HHcy) promotes atherogenesis by modification of histone acetylation patterns and regulation of miRNA expression while the underlying molecular mechanisms are not well known. In this study, we investigated the effects of homocysteine (Hcy) on the expression of histone deacetylase 1 (HDAC1) and tested our hypothesis that Hcy-induced atherosclerosis is mediated by increased HDAC1 expression, which is regulated by miR-34a. The expression of HDAC1 increased and acetylation of histone H3 at lysine 9 (H3K9ac) decreased in the aorta of ApoE mice fed with high methionine diet, whereas miR-34a expression was inhibited. Over-expression of HDAC1 inhibited H3K9ac level and promoted the accumulation of total cholesterol, free cholesterol, and triglycerides in the foam cells. Furthermore, up-regulation of miR-34a reduced HDAC1 expression and inhibited the accumulation of total cholesterol (TC), free cholesterol (FC), and triglycerides (TG) in the foam cells. These data suggest that HDAC1-related H3K9ac plays a key role in Hcy-mediated lipid metabolism disorders, and that miR-34a may be a novel therapeutic target in Hcy-related atherosclerosis. J. Cell. Biochem. 118: 4617-4627, 2017. © 2017 Wiley Periodicals, Inc.

show abstract

mentioning

confidence: 99%

miR‐34a Targets HDAC1‐Regulated H3K9 Acetylation on Lipid Accumulation Induced by Homocysteine in Foam Cells

Zhao

et al. 2017

J of Cellular Biochemistry

View full text Add to dashboard Cite

show abstract

“…Several studies have investigated global histone methylation in human atherosclerotic plaques [6,51,52]. Greißel et al demonstrated that global H3K9me2 and H3K27me2 were significantly decreased in atherosclerotic lesions, while comparable H3K4me2 levels were identified in atherosclerotic and healthy carotid arteries [6].…”

Section: Histone Methylation In Atherosclerosis and Vascular Intimal mentioning

confidence: 99%

“…Paradoxically, the expression of the corresponding histone methyltransferases MLL2 and G9a was increased in advanced atherosclerosis compared to early atherosclerosis [6]. In addition, this research group also demonstrated that H3K4 methylation and H3K9 acetylation were significantly associated with the severity of atherosclerosis [52]. Similarly, Wierda et al also demonstrated that the global level of H3K27me3 was reduced in vessels with advanced atherosclerotic plaques, but this reduction in H3K27me3 level was not accompanied by alterations in the corresponding histone methyltransferase EZH2 or demethylase JMJD3 [51].…”

Section: Histone Methylation In Atherosclerosis and Vascular Intimal mentioning

confidence: 99%

Histone methylation and vascular biology

Wei

Zhu

et al. 2020

Clin Epigenet

View full text Add to dashboard Cite

The vasculature not only transports oxygenated blood, metabolites, and waste products but also serves as a conduit for hormonal communication between distant tissues. Therefore, it is important to maintain homeostasis within the vasculature. Recent studies have greatly expanded our understanding of the regulation of vasculature development and vascular-related diseases at the epigenetic level, including by protein posttranslational modifications, DNA methylation, and noncoding RNAs. Integrating epigenetic mechanisms into the pathophysiologic conceptualization of complex and multifactorial vascular-related diseases may provide promising therapeutic approaches. Several reviews have presented detailed discussions of epigenetic mechanisms not including histone methylation in vascular biology. In this review, we primarily discuss histone methylation in vascular development and maturity, and in vascular diseases.

show abstract

“…Anacardic acid (6-nonadecyl salicylic acid) is another HAT inhibitor with potency toward p300 and cellular p300/CBP associated factor (PCAF) [51]. Recently MG149, a novel analog of anacardic acid, has been developed as a potent and selective inhibitor of the MYST family (Tip60 or KAT5 and MOZ) of HATs [50].…”

Section: Histone Acetyl Transferase Inhibitormentioning

confidence: 99%