Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UNIPROT:P04040 (
Catalase
)
3,577
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
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.
...
PMID:JMJD1A Represses the Development of Cardiomyocyte Hypertrophy by Regulating the Expression of
Catalase
. 3246 96
