Метилирование ретротранспозона Line-1 при атеросклерозе; Перспективы развития фундаментальных наук; Т. 4 : Биология и фундаментальная медицина

書誌詳細
Parent link:Перспективы развития фундаментальных наук=Prospects of Fundamental Sciences Development: сборник научных трудов XIV Международной конференции студентов, аспирантов и молодых ученых, г. Томск, 25-28 апреля 2017 г./ Национальный исследовательский Томский политехнический университет (ТПУ) ; под ред. И. А. Курзиной, Г. А. Вороновой.— , 2017
Т. 4 : Биология и фундаментальная медицина.— 2017.— [С. 151-153]
第一著者: Серебрякова В. В.
その他の著者: Марков А. В. (научный руководитель)
要約:Заглавие с экрана
DNA methylation is one of the perspective but insufficiently studied epigenetic mechanisms which can be involved in atherosclerosis and related cardiovascular disease. Global DNA methylation estimated by the methylation level of retrotransposon LINE-1 in peripheral blood leukocytes (PBLs) was shown to be decreased in coronary heart disease and stroke. The aim of our study was to characterize LINE-1 methylation variability in PBLs of healthy persons (males, n=36), and, PBLs and cells of affected carotid arteries (CACs) of patients with atherosclerosis (males, n=63). LINE-1 methylation analysis was performed using bisulfite pyrosequencing. We showed significant hypomethylation (p<0,05) in both PBLs and CACs of patients in comparison with PBLs of healthy individuals. But there was no significant difference between LINE-1 methylation levels in matched PBLs and CACs of the same patients. Methylation level of LINE-1 in CACs but not in PBLs of patients with atherosclerosis was negatively associated with atherogenic index, which was partly in contrast with recent findings. Mild decrease in LINE-1 methylation with age was observed in PBLs of only healthy men. Absence of the same association in patients with atherosclerosis can be explained by stronger relation between LINE-1 methylation with the severity of the disease rather than age.
言語:ロシア語
出版事項: 2017
主題:
オンライン・アクセス:http://earchive.tpu.ru/handle/11683/44883
フォーマット: 電子媒体 図書の章
KOHA link:https://koha.lib.tpu.ru/cgi-bin/koha/opac-detail.pl?biblionumber=625087

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