Метилирование ретротранспозона Line-1 при атеросклерозе

Bibliographic Details
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]
Main Author: Серебрякова В. В.
Other Authors: Марков А. В. (727)
Summary: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.
Published: 2017
Subjects:
Online Access:http://earchive.tpu.ru/handle/11683/44883
Format: Electronic Book Chapter
KOHA link:https://koha.lib.tpu.ru/cgi-bin/koha/opac-detail.pl?biblionumber=625087