Iribe2006_CaMKIIkineticsModel

ABSTRACT:

This a model from the article:
Modulatory effect of calmodulin-dependent kinase II (CaMKII) on sarcoplasmicreticulum Ca2+ handling and interval-force relations: a modelling study.
Iribe G, Kohl P, Noble D. Philos Transact A Math Phys Eng Sci 2006 May 15;364(1842):1107-33 16608699 ,
Abstract:
We hypothesize that slow inactivation of Ca2+/calmodulin-dependent kinase II(CaMKII) and its modulatory effect on sarcoplasmic reticulum (SR) Ca2+ handlingare important for various interval-force (I-F) relations, in particular for thebeat interval dependency in transient alternans during the decay ofpost-extrasystolic potentiation. We have developed a mathematical model of asingle cardiomyocyte to integrate various I-F relations, including alternans, byincorporating a conceptual CaMKII kinetics model into the SR Ca2+ handlingmodel. Our model integrates I-F relations, such as the beat interval-dependenttwitch force duration, restitution and potentiation, positive staircasephenomenon and alternans. We found that CaMKII affects more or less all I-Frelations, and it is a key factor for integration of the various I-F relationsin our model. Alternans arises, in the model, out of a steep relation between SRCa2+ load and release, owing to SR load-dependent changes in the releasabilityof Ca2+ via the ryanodine receptor. Beat interval-dependent CaMKII activity,owing to its kinetic properties and amplifying effect on SR Ca2+ load dependencyof Ca2+ release, replicated the beat interval dependency of alternans, asobserved experimentally. Additionally, our model enabled reproduction of theeffects of various interventions on alternans, such as the slowing oraccelerating of Ca2+ release and/or uptake. We conclude that a slowtime-dependent factor, represented in the model by CaMKII, is important for theintegration of I-F relations, including alternans, and that our model offers auseful tool for further analysis of the roles of integrative Ca2+ handling inmyocardial I-F relations.

This model was taken from the CellML repository and automatically converted to SBML.
The original model was: Iribe G, Kohl P, Noble D. (2006) - version=1.0
The original CellML model was created by:
Penny Noble
[e-mail]
The University of Oxford

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To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.

ORGANISM(S): Mammalia

SUBMITTER: Camille Laibe 

PROVIDER: MODEL1006230085 | biostudies-other |

SECONDARY ACCESSION(S): 16608699

REPOSITORIES: biostudies-other