Fibrogenesis Genes and Susceptibility to Coronary Atherosclerosis

Goncharova, I. A.; Печерина, Т. Б.; Марков, А. В.; Кашталап, В В; Tarasenko, N. V.; Puzyrev, V P; Барбараш, О. Л.

doi:10.18087/cardio.2018.8.10160

Cited by 6 publications

(1 citation statement)

References 38 publications

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“…Of crucial importance, the current study obtained evidence verifying the existence of low expression of CDKN2B-AS1 in clinical atherosclerotic plaque tissues, while elucidating the potential anti-atherogenic role of CDKN2B-AS1. In line with our study, it has been reported that the susceptibility to coronary atherosclerosis and the prognosis of disease progression involve extracellular matrix metabolism and fibrogenesis whereby CDKN2B-AS1 assumes an essential role [27]. Additionally, the results of the current study also indicated that ADAM10 was highly expressed in atherosclerotic plaque tissues and ox-LDL-exposed THP-1 macrophages.…”

Section: Discussionsupporting

confidence: 90%

Long non-coding RNA CDKN2B-AS1 reduces inflammatory response and promotes cholesterol efflux in atherosclerosis by inhibiting ADAM10 expression

Han

Sun

et al. 2019

Aging

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Introduction: Long non-coding RNAs (lncRNAs) play key roles in the development of atherosclerosis through the inflammatory pathway. This study aimed to investigate the role of lncRNA cyclin-dependent kinase inhibitor 2B antisense RNA 1 (CDKN2B-AS1) in atherosclerosis via its function in A disintegrin and metalloprotease 10 (ADAM10). Methods: Initially, the expression of CDKN2B-AS1 and ADAM10 in atherosclerotic plaque tissues and THP-1 macrophage-derived foam cells was determined, after which the cholesterol efflux rate of macrophages was calculated. Interaction between CDKN2B-AS1 and ADAM10 was analyzed, after which, expression of CDKN2B-AS1 and ADAM10 were altered to explore their effects on inflammatory response and cholesterol efflux. The aforementioned findings were further intended to be validated by the atherosclerosis mouse model experiments. Results: Atherosclerotic plaque tissue and THP-1 macrophage-derived foam cells exhibited downregulated CDKN2B-AS1 and upregulated ADAM10. Upon overexpressing CDKN2B-AS1 or silencing ADAM10, lipid accumulation was reduced and cholesterol efflux was increased. CDKN2B-AS1 located in the nucleus could bind to DNA methyltransferase 1 (DNMT1) to enhance methylation of ADAM10 promoter, leading to suppressed atherosclerotic inflammatory response and promoted cholesterol efflux. Conclusion: Altogether, lncRNA CDKN2B-AS1 can inhibit the transcription of ADAM10 via DNMT1-mediated ADAM10 DNA methylation, consequently preventing inflammatory response of atherosclerosis and promoting cholesterol efflux.

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Section: Discussionsupporting

confidence: 90%