JMJD1A Represses the Development of Cardiomyocyte Hypertrophy by Regulating the Expression of Catalase.

JMJD1A Represses the Development of Cardiomyocyte Hypertrophy by Regulating the Expression of Catalase. Biomed Res Int. 2020;2020:5081323 Authors: Zang R, Tan Q, Zeng F, Wang D, Yu S, Wang Q Abstract 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 t...
Source: Biomed Res - Category: Research Authors: Tags: Biomed Res Int Source Type: research

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(Technical University of Munich (TUM)) An adenovirus infection can be potentially life-threatening, especially for children after a stem cell transplant. Virologists at the Technical University of Munich (TUM) and the German Research Center for Environmental Health Helmholtz Zentrum M ü nchen have successfully shown that a previously approved medication used in cancer treatment could help inhibit this virus infection. Due to the special mechanism of action, the virus cannot develop defence strategies.
Source: EurekAlert! - Medicine and Health - Category: International Medicine & Public Health Source Type: news
Abstract Adeno-associated virus (AAV) has emerged as the vector of choice for delivering genes to the mammalian retina. From the first gene therapy to receive FDA approval for the inherited retinal disease (Luxturna™) to more recent clinical trials using microbial opsins to regain light sensitivity, therapeutic transgenes rely on AAV vectors for safe and efficient gene delivery to retinal cells. Such vectors are administered to the retina via subretinal (SR) injection or intravitreal (IVT) injection routes depending on the targeted retinal cell type. An attractive target for gene therapy is the fovea, bearin...
Source: Mol Biol Cell - Category: Molecular Biology Authors: Tags: Methods Mol Biol Source Type: research
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Source: Mol Biol Cell - Category: Molecular Biology Authors: Tags: Methods Mol Biol Source Type: research
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Source: Viruses - Category: Virology Authors: Tags: Article Source Type: research
ConclusionsThe presentation of our patients raises the possibility that hypertrophic cardiomyopathy may be an additional feature of the clinical syndrome associated withUCHL1 mutations, and highlights the importance of cardiac follow-up and treatment in neurodegenerative disease associated withUCHL1 mutations.
Source: Journal of Neurology - Category: Neurology Source Type: research
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Source: Free Radical Biology and Medicine - Category: Biology Authors: Tags: Free Radic Biol Med Source Type: research
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Source: Journal of Molecular Medicine - Category: Molecular Biology Source Type: research
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Source: - Category: Pediatrics Authors: Tags: Uncategorized Source Type: news
Mutations in thin filament regulatory proteins that cause hypertrophic cardiomyopathy (HCM) increase myofilament Ca2+ sensitivity. Mouse models exhibit increased Ca2+ buffering and arrhythmias, and we hypothesized that these changes are primary effects of the mutations (independent of compensatory changes) and that increased Ca2+ buffering and altered Ca2+ handling contribute to HCM pathogenesis via activation of Ca2+-dependent signaling. Here, we determined the primary effects of HCM mutations on intracellular Ca2+ handling and Ca2+-dependent signaling in a model system possessing Ca2+-handling mechanisms and contractile ...
Source: Journal of Biological Chemistry - Category: Chemistry Authors: Tags: Molecular Bases of Disease Source Type: research
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