ArticleIn vitro cellular & developmental biology. Animal2016
Calmodulin kinase II inhibitor regulates calcium homeostasis changes caused by acute β-adrenergic receptor agonist stimulation in mouse ventricular myocytes.
Article in In vitro cellular & developmental biology. Animal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 4 citations in OpenAlex.
- CaMK II in Cardiovascular Diseases, Especially CaMK II-δ: Friends or Enemies.Drug design, development and therapy · 2024Review
- L-type CaPhysiological reports · 2022Article
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Authors and funding
9 authors at 2 institutions in 1 country.
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Abstract
Ca(2+)/calmodulin-dependent kinase II (CaMKII) is an important regulatory molecule under chronic β-adrenergic receptor agonist stimulation but cardiac diseases also occur when β-adrenergic elevated acutely in the circulation, of which the most harmful is lethal arrhythmia. The purpose of this study was to explore the effects of acute isoproterenol (ISO) stimulation on intracellular calcium handling and evaluate whether CaMKII inhibitor may change the effects caused by isoproterenol. Mouse ventricular myocytes were acutely isolated by enzymatic method and divided into four groups: control group, ISO group, KN-93 group, ISO + KN-93 group. The whole-cell patch clamp was used to study the effect of ISO and KN-93 on L-type calcium current (IL-Ca) in isolated ventricular myocytes. The technology of laser scanning confocal microscopy was used to record cardiomyocyte calcium transients after ISO and KN-93 were used. ISO significantly increased current density of IL-Ca (p < 0.01) and decreased the half activation voltage (p < 0.01), half inactivation voltage (p < 0.01), and the recovery time constant (p < 0.01). In the presence of CaMKII inhibitor, KN-93 decreased the increased current density of IL-Ca (p < 0.05), increased the reduced half activation voltage caused by ISO (p < 0.01), and prolonged the shortened recovery time constant caused by ISO (p < 0.01). In addition, KN-93 alone can change the activation, inactivation, and recovery kinetics of L-type calcium channels. Moreover, ISO significantly increased the Ca(2+) transient amplitude during both stimulation frequencies (0.5 Hz: p < 0.01, 1 Hz: p < 0.01) and was easy to induce calcium disorders; in the presence of KN-93, these changes were weakened (0.5 Hz: p < 0.05, 1 Hz: p < 0.05). Therefore, changes of the calcium homeostasis in cardiomyocytes caused by ISO can be adjusted by KN-93, thus KN-93 plays a vital role in regulating calcium homeostasis changes caused by ISO.
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