ArticleMolecular biology reports2012
Analysis of Na(+)/Ca (2+) exchanger (NCX) function and current in murine cardiac myocytes during heart failure.
Article in Molecular biology reports, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 18 citations in OpenAlex.
- Skeletal and cardiac muscle calcium transport regulation in health and disease.Bioscience reports · 2022Review
- Stress-driven cardiac calcium mishandling via a kinase-to-kinase crosstalk.Pflugers Archiv : European journal of physiology · 2021Review
- Cholinergic stimulation improves electrophysiological rate adaptation during pressure overload-induced heart failure in rats.American journal of physiology. Heart and circulatory physiology · 2020Article
- The Effects of Mechanical Preload on Transmural Differences in Mechano-Calcium-Electric Feedback in Single Cardiomyocytes: Experiments and Mathematical Models.Frontiers in physiology · 2020Article
- Cardiac dynamics: Alternans and arrhythmogenesis.Journal of arrhythmia · 2016Review
- Regulation of cardiomyocyte autophagy by calcium.American journal of physiology. Endocrinology and metabolism · 2016Review
- Distinctive profile of IsomiR expression and novel microRNAs in rat heart left ventricle.PloS one · 2013Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Na(+)/Ca(2+) exchanger (NCX) plays important roles in cardiac electrical activity and calcium homeostasis. NCX current (I(NCX)) shows transmural gradient across left ventricle in many species. Previous studies demonstrated that NCX expression was increased and transmural gradient of I(NCX) was disrupted in failing heart, but the mechanisms underlying I(NCX) remodeling still remain unknown. In present study, we used patch clamp technique to record I(NCX) from subepicardial (EPI) myocytes and subendocardial (ENDO) myocytes isolated from sham operation (SO) mice and heart failure (HF) mice. Our results showed that I(NCX) was higher in normal EPI cells compared with that in ENDO, whatever for forward mode or reverse mode. In HF group, I(NCX) was significantly up-regulated, but EPI-ENDO difference was disrupted because of a more increase of I(NCX) in ENDO myocytes. In order to explore the molecular mechanism underlying remodeling of I(NCX) in failing heart, we detected the protein expression of NCX1 and Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) by Western blot. We found that CaMKII activity was dramatically enhanced and parallel with the expression of NCX1 in failing heart. Our study demonstrated that transmural gradient of I(NCX) existed in murine left ventricle, and increased activity of CaMKII should account for I(NCX) remodeling in failing heart.
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