ArticleJournal of translational medicine2012
Ca²+-regulatory proteins in cardiomyocytes from the right ventricle in children with congenital heart disease.
Article in Journal of translational medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Clinical presentation of calmodulin mutations: the International Calmodulinopathy Registry.European heart journal · 2023Observational
- Blocking transferrin receptor inhibits the growth of lung adenocarcinoma cells in vitro.Thoracic cancer · 2018Article
- Current Knowledge and Recent Advances of Right Ventricular Molecular Biology and Metabolism from Congenital Heart Disease to Chronic Pulmonary Hypertension.BioMed research international · 2018Review
- Hydrogen Sulfide Inhibits High-Salt Diet-Induced Myocardial Oxidative Stress and Myocardial Hypertrophy in Dahl Rats.Frontiers in pharmacology · 2017Article
- Cellular and molecular basis of RV hypertrophy in congenital heart disease.Heart (British Cardiac Society) · 2016Review
- Identification and Functional Characterization of a Novel CACNA1C-Mediated Cardiac Disorder Characterized by Prolonged QT Intervals With Hypertrophic Cardiomyopathy, Congenital Heart Defects, and Sudden Cardiac Death.Circulation. Arrhythmia and electrophysiology · 2015Article
- Identification of Region-Specific Myocardial Gene Expression Patterns in a Chronic Swine Model of Repaired Tetralogy of Fallot.PloS one · 2015Article
- Heart failure in congenital heart disease: the role of genes and hemodynamics.Pflugers Archiv : European journal of physiology · 2014Review
- Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHypoxia and hypertrophy are the most frequent pathophysiological consequence of congenital heart disease (CHD) which can induce the alteration of Ca2+-regulatory proteins and inhibit cardiac contractility. Few studies have been performed to examine Ca2+-regulatory proteins in human cardiomyocytes from the hypertrophic right ventricle with or without hypoxia.
methodsRight ventricle tissues were collected from children with tetralogy of Fallot [n = 25, hypoxia and hypertrophy group (HH group)], pulmonary stenosis [n = 25, hypertrophy group (H group)], or small isolated ventricular septal defect [n = 25, control group (C group)] during open-heart surgery. Paraffin sections of tissues were stained with 3,3'-dioctadecyloxacarbocyanine perchlorate to measure cardiomyocyte size. Expression levels of Ca2+-regulatory proteins [sarcoplasmic reticulum Ca2+-ATPase (SERCA2a), ryanodine receptor (RyR2), sodiumcalcium exchanger (NCX), sarcolipin (SLN) and phospholamban (PLN)] were analysed by means of real-time PCR, western blot, or immunofluorescence. Additionally, phosphorylation level of RyR and PLN and activity of protein phosphatase (PP1) were evaluated using western blot.
resultsMild cardiomyocyte hypertrophy of the right ventricle in H and HH groups was confirmed by comparing cardiomyocyte size. A significant reduction of SERCA2a in mRNA (P<0.01) was observed in the HH group compared with the C group. The level of Ser16-phosphorylated PLN was down-regulated (P<0.01) and PP1 was increased (P<0.01) in the HH group compared to that in the C group.
conclusionsThe decreased SERCA2a mRNA may be a biomarker of the pathological process in the early stage of cyanotic CHD with the hypertrophic right ventricle. A combination of hypoxia and hypertrophy can induce the adverse effect of PLN-Ser16 dephosphorylation. Increased PP1 could result in the decreased PLN-Ser16 and inhibition of PP1 is a potential therapeutic target for heart dysfunction in pediatrics.
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