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LINE-1 retrotransposon demethylation is associated to atherosclerotic plaques destabilization

https://doi.org/10.25557/2073-7998.2020.05.50-51

Abstract

We analyzed the LINE-1 methylation level in carotid atherosclerotic plaques, macrophages and smooth muscle cells isolated from plaques and in the blood leukocytes of patients with clinically significant atherosclerosis and leukocytes of healthy donors. A reduced level of LINE-1 methylation in atherosclerotic plaques was detected compared to leukocytes, as well as it was associated with the histological features of carotid plaque instability.

About the Authors

D. V. Sharysh
Research Institute of Medical Genetics, Tomsk National Research Medical Center of the Russian Academy of Sciences
Russian Federation


A. V. Markov
Research Institute of Medical Genetics, Tomsk National Research Medical Center of the Russian Academy of Sciences
Russian Federation


A. A. Sleptcov
Research Institute of Medical Genetics, Tomsk National Research Medical Center of the Russian Academy of Sciences
Russian Federation


N. R. Valiakhmetov
Research Institute of Medical Genetics, Tomsk National Research Medical Center of the Russian Academy of Sciences
Russian Federation


I. A. Koroleva
Research Institute of Medical Genetics, Tomsk National Research Medical Center of the Russian Academy of Sciences
Russian Federation


A. A. Kazantsev
Research Institute for Complex Issues of Cardiovascular Diseases
Russian Federation


O. L. Barbarash
Research Institute for Complex Issues of Cardiovascular Diseases
Russian Federation


M. S. Nazarenko
Research Institute of Medical Genetics, Tomsk National Research Medical Center of the Russian Academy of Sciences
Russian Federation


Review

For citations:


Sharysh D.V., Markov A.V., Sleptcov A.A., Valiakhmetov N.R., Koroleva I.A., Kazantsev A.A., Barbarash O.L., Nazarenko M.S. LINE-1 retrotransposon demethylation is associated to atherosclerotic plaques destabilization. Medical Genetics. 2020;19(5):50-51. (In Russ.) https://doi.org/10.25557/2073-7998.2020.05.50-51

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ISSN 2073-7998 (Print)