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JMJD1A Represses the Development of Cardiomyocyte Hypertrophy by Regulating the Expression of Catalase
Joint Authors
Zang, Rongjia
Tan, Qingyun
Zeng, Fanrong
Wang, Dongwei
Yu, Shuang
Wang, Qingdong
Source
Issue
Vol. 2020, Issue 2020 (31 Dec. 2020), pp.1-14, 14 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2020-05-13
Country of Publication
Egypt
No. of Pages
14
Main Subjects
Abstract EN
The histone demethylase JMJD family is involved in various physiological and pathological functions.
However, the roles of JMJD1A in the cardiovascular system remain unknown.
Here, we studied the function of JMJD1A in cardiac hypertrophy.
The mRNA and protein levels of JMJD1A were significantly downregulated in the hearts of human patients with hypertrophic cardiomyopathy and the hearts of C57BL/6 mice underwent cardiac hypertrophy induced by transverse aortic constriction (TAC) surgery or isoproterenol (ISO) infusion.
In neonatal rat cardiomyocytes (NRCMs), siRNA-mediated JMJD1A knockdown facilitated ISO or angiotensin II-induced increase in cardiomyocyte size, protein synthesis, and expression of hypertrophic fetal genes, including atrial natriuretic peptide (Anp), brain natriuretic peptide (Bnp), and Myh7.
By contrast, overexpression of JMJD1A with adenovirus repressed the development of ISO-induced cardiomyocyte hypertrophy.
We observed that JMJD1A reduced the production of total cellular and mitochondrial levels of reactive oxygen species (ROS), which was critically involved in the effects of JMJD1A because either N-acetylcysteine or MitoTEMPO treatment blocked the effects of JMJD1A deficiency on cardiomyocyte hypertrophy.
Mechanism study demonstrated that JMJD1A promoted the expression and activity of Catalase under basal condition or oxidative stress.
siRNA-mediated loss of Catalase blocked the protection of JMJD1A overexpression against ISO-induced cardiomyocyte hypertrophy.
These findings demonstrated that JMJD1A loss promoted cardiomyocyte hypertrophy in a Catalase and ROS-dependent manner.
American Psychological Association (APA)
Zang, Rongjia& Tan, Qingyun& Zeng, Fanrong& Wang, Dongwei& Yu, Shuang& Wang, Qingdong. 2020. JMJD1A Represses the Development of Cardiomyocyte Hypertrophy by Regulating the Expression of Catalase. BioMed Research International،Vol. 2020, no. 2020, pp.1-14.
https://search.emarefa.net/detail/BIM-1134445
Modern Language Association (MLA)
Zang, Rongjia…[et al.]. JMJD1A Represses the Development of Cardiomyocyte Hypertrophy by Regulating the Expression of Catalase. BioMed Research International No. 2020 (2020), pp.1-14.
https://search.emarefa.net/detail/BIM-1134445
American Medical Association (AMA)
Zang, Rongjia& Tan, Qingyun& Zeng, Fanrong& Wang, Dongwei& Yu, Shuang& Wang, Qingdong. JMJD1A Represses the Development of Cardiomyocyte Hypertrophy by Regulating the Expression of Catalase. BioMed Research International. 2020. Vol. 2020, no. 2020, pp.1-14.
https://search.emarefa.net/detail/BIM-1134445
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1134445