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ISSN 2522-9028 (Print)
ISSN 2522-9036 (Online)
DOI: https://doi.org/10.15407/fz

Fiziologichnyi Zhurnal

is a scientific journal issued by the

Bogomoletz Institute of Physiology
National Academy of Sciences of Ukraine

Editor-in-chief: V.F. Sagach

The journal was founded in 1955 as
1955 – 1977 "Fiziolohichnyi zhurnal" (ISSN 0015 – 3311)
1978 – 1993 "Fiziologicheskii zhurnal" (ISSN 0201 – 8489)
1994 – 2016 "Fiziolohichnyi zhurnal" (ISSN 0201 – 8489)
2017 – "Fiziolohichnyi zhurnal" (ISSN 2522-9028)

Fiziol. Zh. 2024; 70(1): 52-59


CHANGES IN THE EXPRESSION OF LONG NON-CODING RNAS H19, TUG1, GAS5, MIAT DURING MYOCARDIAL ISCHEMIA-REPERFUSION

M. Khetsuriani, T.I. Drevytska, A.M. Shysh

    Bogomoletz Institute of Physiology, National Academy of Sciences of Ukraine, Kyiv, Ukraine
DOI: https://doi.org/10.15407/fz70.01.052


Abstract

Long non-coding RNAs (lncRNAs) are the most numerous group of transcripts performing various functions, including the development of cardiovascular pathologies. We investigated the changes in expression of four long non-coding RNAs (H19, TUG1, GAS5, MIAT) under conditions of anoxia-reoxygenation in neonatal rat cardiomyocyte culture and ischemia-reperfusion in adult Wistar rats. A significant decrease in the expression of all four long non-coding RNAs in cell culture under experimental conditions was established. The regime of prolonged anoxia-reoxygenation led to a sharp increase in the expression level of long non-coding RNA MIAT by twice, but compared to normoxia, these changes were not significant. After ischemia-reperfusion in rat myocardium, the content of long non-coding RNA TUG1 increased by 22 times, while the expression of H19 decreased by 3.79 times, and in rat plasma, the expression of long non-coding RNA MIAT increased by 3.79 times. The obtained results allow considering long non-coding RNAs H19 and TUG1 as potential targets in ischemic myocardial injury, and MIAT as a biomarker of cardiovascular pathologies.

Keywords: long non-coding RNAs; ischemia; heart; myocardium; cardiomyocyte; H19; MIAT; TUG1.

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