FTO overexpression inhibits apoptosis of hypoxia/reoxygenation-treated myocardial cells by regulating m6A modification of Mhrt.

Szczegóły
Abstrakt

Tytuł:: FTO overexpression inhibits apoptosis of hypoxia/reoxygenation-treated myocardial cells by regulating m6A modification of Mhrt.
Autorzy:: Shen W; Department of Cardiovascular, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, No.17 Lujiang Road, Hefei, 230001, China.
Li H; Department of Gerontology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, 230001, China.
Su H; Department of Cardiovascular, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, No.17 Lujiang Road, Hefei, 230001, China.
Chen K; Department of Cardiovascular, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, No.17 Lujiang Road, Hefei, 230001, China.
Yan J; Department of Cardiovascular, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, No.17 Lujiang Road, Hefei, 230001, China. .
Źródło:: Molecular and cellular biochemistry [Mol Cell Biochem] 2021 May; Vol. 476 (5), pp. 2171-2179. Date of Electronic Publication: 2021 Feb 06.
Typ publikacji:: Journal Article
Język:: English
Imprint Name(s):: Publication: New York : Springer
Original Publication: The Hague, Dr. W. Junk B. V. Publishers.
MeSH Terms:: Apoptosis*
Gene Expression Regulation, Enzymologic*
Alpha-Ketoglutarate-Dependent Dioxygenase FTO/*biosynthesis
Myocardial Reperfusion Injury/*metabolism
Myocardium/*metabolism
Myocytes, Cardiac/*metabolism
RNA, Long Noncoding/*metabolism
Alpha-Ketoglutarate-Dependent Dioxygenase FTO/genetics ; Animals ; Male ; Methylation ; Mice ; Myocardial Reperfusion Injury/genetics ; Myocardial Reperfusion Injury/pathology ; Myocardium/pathology ; Myocytes, Cardiac/pathology ; RNA, Long Noncoding/genetics
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Grant Information:: 2016080802D113 The special projects of development in local science and technology guided by the central government; 1808085MH281 Natural Science Foundation of Anhui Province; WK9110000046 New Medicine of University of Science and Technology of China
Contributed Indexing:: Keywords: Apoptosis; FTO; Heart failure; Mhrt; m6A modification
Substance Nomenclature:: 0 (RNA, Long Noncoding)
EC 1.14.11.- (FTO protein, mouse)
EC 1.14.11.33 (Alpha-Ketoglutarate-Dependent Dioxygenase FTO)
Entry Date(s):: Date Created: 20210206 Date Completed: 20210728 Latest Revision: 20210728
Update Code:: 20240104
DOI:: 10.1007/s11010-021-04069-6
PMID:: 33548009
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Heart failure (HF) is the end stage of many cardiovascular diseases and seriously threatens people's health. This article aimed to explore the biological role of fat-mass and obesity-associated gene (FTO) in HF. We constructed HF mouse model by transverse aortic constriction or intraperitoneal injection of doxorubicin. Mouse myocardial cells were exposed to hypoxia/reoxygenation (H/R). FTO and Mhrt were downregulated in heart tissues of HF mice. HF mice exhibited an increase in the total levels of N 6 methyladenosine (m 6 A) and the m 6 A levels of Mhrt. Moreover, FTO overexpression caused an upregulation of Mhrt and reduced m 6 A modification of Mhrt in the H/R-treated myocardial cells. FTO upregulation repressed apoptosis of H/R-treated myocardial cells. FTO knockdown had the opposite results. Mhrt overexpression reduced apoptosis of H/R-treated myocardial cells. Moreover, the influence conferred by FTO upregulation was abolished by Mhrt knockdown. In conclusion, our data demonstrate that FTO overexpression inhibits apoptosis of hypoxia/reoxygenation-treated myocardial cells by regulating m6A modification of Mhrt. Thus, FTO may be a target gene for HF treatment.

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