دورية أكاديمية
أعرض في EDS

Rate-dependent Ca2+ signalling underlying the force-frequency response in rat ventricular myocytes: a coupled electromechanical modeling study.

التفاصيل البيبلوغرافية
العنوان: Rate-dependent Ca2+ signalling underlying the force-frequency response in rat ventricular myocytes: a coupled electromechanical modeling study.
المؤلفون: Krishna A; Department of Electrical and Computer Engineering, Rice University, Houston, Texas, USA. jwc@rice.edu., Valderrábano M, Palade PT, Clark JW Jr
المصدر: Theoretical biology & medical modelling [Theor Biol Med Model] 2013 Sep 10; Vol. 10, pp. 54. Date of Electronic Publication: 2013 Sep 10.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: BioMed Central Country of Publication: England NLM ID: 101224383 Publication Model: Electronic Cited Medium: Internet ISSN: 1742-4682 (Electronic) Linking ISSN: 17424682 NLM ISO Abbreviation: Theor Biol Med Model Subsets: MEDLINE
أسماء مطبوعة: Original Publication: [London] : BioMed Central, 2004-2021
مواضيع طبية MeSH: Calcium Signaling*/drug effects , Electrophysiological Phenomena*/drug effects, Heart Ventricles/*cytology , Myocytes, Cardiac/*physiology, Animals ; Biomechanical Phenomena/drug effects ; Calcineurin/metabolism ; Calcium/metabolism ; Calcium-Calmodulin-Dependent Protein Kinase Type 2/metabolism ; Calmodulin/metabolism ; Cyclic AMP/metabolism ; Cyclic GMP/metabolism ; Dihydropyridines/pharmacology ; Intracellular Space/drug effects ; Intracellular Space/metabolism ; Kinetics ; Models, Biological ; Myocardial Contraction/drug effects ; Myocytes, Cardiac/drug effects ; Rats ; Receptors, Adrenergic, beta/metabolism ; Ryanodine Receptor Calcium Release Channel/metabolism ; Sarcomeres/drug effects ; Sarcomeres/metabolism ; Sarcoplasmic Reticulum Calcium-Transporting ATPases/metabolism ; Signal Transduction/drug effects
مستخلص: Background: Rate-dependent effects on the Ca2+ sub-system in a rat ventricular myocyte are investigated. Here, we employ a deterministic mathematical model describing various Ca2+ signalling pathways under voltage clamp (VC) conditions, to better understand the important role of calmodulin (CaM) in modulating the key control variables Ca2+/calmodulin-dependent protein kinase-II (CaMKII), calcineurin (CaN), and cyclic adenosine monophosphate (cAMP) as they affect various intracellular targets. In particular, we study the frequency dependence of the peak force generated by the myofilaments, the force-frequency response (FFR).
Methods: Our cell model incorporates frequency-dependent CaM-mediated spatially heterogenous interaction of CaMKII and CaN with their principal targets (dihydropyridine (DHPR) and ryanodine (RyR) receptors and the SERCA pump). It also accounts for the rate-dependent effects of phospholamban (PLB) on the SERCA pump; the rate-dependent role of cAMP in up-regulation of the L-type Ca2+ channel (ICa,L); and the enhancement in SERCA pump activity via phosphorylation of PLB.
Results: Our model reproduces positive peak FFR observed in rat ventricular myocytes during voltage-clamp studies both in the presence/absence of cAMP mediated β-adrenergic stimulation. This study provides quantitative insight into the rate-dependence of Ca2+-induced Ca2+-release (CICR) by investigating the frequency-dependence of the trigger current (ICa,L) and RyR-release. It also highlights the relative role of the sodium-calcium exchanger (NCX) and the SERCA pump at higher frequencies, as well as the rate-dependence of sarcoplasmic reticulum (SR) Ca2+ content. A rigorous Ca2+ balance imposed on our investigation of these Ca2+ signalling pathways clarifies their individual roles. Here, we present a coupled electromechanical study emphasizing the rate-dependence of isometric force developed and also investigate the temperature-dependence of FFR.
Conclusions: Our model provides mechanistic biophysically based explanations for the rate-dependence of CICR, generating useful and testable hypotheses. Although rat ventricular myocytes exhibit a positive peak FFR in the presence/absence of beta-adrenergic stimulation, they show a characteristic increase in the positive slope in FFR due to the presence of Norepinephrine or Isoproterenol. Our study identifies cAMP-mediated stimulation, and rate-dependent CaMKII-mediated up-regulation of ICa,L as the key mechanisms underlying the aforementioned positive FFR.
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المشرفين على المادة: 0 (Calmodulin)
0 (Dihydropyridines)
0 (Receptors, Adrenergic, beta)
0 (Ryanodine Receptor Calcium Release Channel)
7M8K3P6I89 (1,4-dihydropyridine)
E0399OZS9N (Cyclic AMP)
EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinase Type 2)
EC 3.1.3.16 (Calcineurin)
EC 3.6.3.8 (Sarcoplasmic Reticulum Calcium-Transporting ATPases)
H2D2X058MU (Cyclic GMP)
SY7Q814VUP (Calcium)
تواريخ الأحداث: Date Created: 20130912 Date Completed: 20140618 Latest Revision: 20240321
رمز التحديث: 20240321
مُعرف محوري في PubMed: PMC3848742
DOI: 10.1186/1742-4682-10-54
PMID: 24020888
قاعدة البيانات: MEDLINE
الوصف
تدمد:1742-4682
DOI:10.1186/1742-4682-10-54