Modelling mechanism of calcium oscillations in pancreatic acinar cells

Manhas, Neeraj; Pardasani, Kamal Raj

doi:10.1007/s10863-014-9561-0

Cited by 47 publications

(10 citation statements)

References 113 publications

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“…1,2 Attempts are reported in the literature for the study of calcium regulation in neuron cell, astrocyte cell, fibroblast cell, oocyte cell, acinar, etc. [3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19] But very few attempts are reported in the literature for the study of calcium dynamics in myocytes. 1,2,20,21 Most of the studies reported on calcium diffusion in myocytes are experimental.…”

Section: Introductionmentioning

confidence: 99%

Finite element model to study two dimensional unsteady state calcium distribution in cardiac myocytes

Pathak

Adlakha

2016

Alexandria Journal of Medicine

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The calcium signaling plays a crucial role in expansion and contraction of cardiac myocytes. This calcium signaling is achieved by calcium diffusion, buffering mechanisms and influx in cardiac myocytes. The various calcium distribution patterns required for achieving calcium signaling in myocytes are still not well understood. In this paper an attempt has been made to develop a model of calcium distribution in myocytes incorporating diffusion of calcium, point source and excess buffer approximation. The model has been developed for a two dimensional unsteady state case. Appropriate boundary conditions and initial condition have been framed. The finite element method has been employed to obtain the solution. The numerical results have been used to study the effect of buffers and source amplitude on calcium distribution in myocytes. Ó 2015 Alexandria University Faculty of Medicine. Production and hosting by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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Section: Introductionmentioning

confidence: 99%

Finite element model to study two dimensional unsteady state calcium distribution in cardiac myocytes

Pathak

Adlakha

2016

Alexandria Journal of Medicine

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“…Although RYRs might be involved in Ca 2+ oscillations (Kannan et al, 1997;McHale et al, 2006;Nakayama et al, 2005;Plummer et al, 2011), studies suggest that Ca 2+ oscillations are mainly generated by the activation of IP3R release channels in many cell types (Abou-Saleh et al, 2013;Berridge, 2007;Hruby et al, 2008;Manhas and Pardasani, 2014;Martin-Cano et al, 2009;Tamarina et al, 2005;Tamashiroand Yoshino, 2014). Our results suggest that the Ca 2+ oscillations induced by the stretching of mouse bladder smooth myocytes was mainly mediated the activation of IP3Rs by NO production, although it was impossible to completely exclude the involvement of RYRs.…”

Section: Discussionmentioning

confidence: 99%

Nitric oxide mediates stretch-induced Ca2+ oscillation in smooth muscle

Zheng

Zhai

Chen

et al. 2016

Journal of Cell Science

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The stretching of smooth muscle tissue modulates contraction through augmentation of Ca 2+ transients, but the mechanism underlying stretch-induced Ca 2+ transients is still unknown. We found that mechanical stretching and maintenance of mouse urinary bladder smooth muscle strips and single myocytes at 30% and 18% beyond the initial length, respectively, resulted in Ca 2+ oscillations. Experiments indicated that mechanical stretching remarkably increased the production of nitric oxide (NO) as well as the amplitude and duration of muscle contraction. Stretch-induced Ca 2+ oscillations and contractility increases were completely abolished by the NO inhibitor L-NAME or eNOS (also known as NOS3) gene inactivation. Moreover, exposure of eNOS-knockout myocytes to exogenous NO donor induced Ca 2+ oscillations. The stretch-induced Ca 2+ oscillations were greatly inhibited by the selective inositol 1,4,5-trisphosphate receptor (IP3R) inhibitor xestospongin C and partially inhibited by ryanodine. Moreover, the stretch-induced Ca 2+ oscillations were also suppressed by the phosphoinositide 3-kinase (PI3K) inhibitor LY294002, but not by the soluble guanylyl cyclase (sGC) inhibitor ODQ. These results suggest that stretching myocyte and maintenance at a certain length results in Ca 2+ oscillations that are NO dependent , and sGC and cGMP independent, and results from the activation of PI3K in smooth muscle.

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“…Pathak et al [18] have developed a two dimensional mathematical model to understand Ca 2+ signaling process in cardiac myocyte but they have not considered the impact of IP 3 dynamics in their model. There are other studies of different cells in literature like hepatocytes [19], neurons [20,21], astrocytes [22,23], fibroblasts [24,25], pancreatic acinar [26,27] and oocytes [28]. But in the existing literature, many mathematical work on Ca 2+ signaling in cardiac myocyte have not paid attention on the role of IP 3 signaling in their mathematical model [29] while those works which state about the impact of IP 3 signaling on Ca 2+ signaling are experimental [30,31,32].…”

Section: Introductionmentioning

confidence: 99%

Nonlinear Dynamic Modeling of 2-Dimensional Interdependent Calcium and Inositol 1,4,5-Trisphosphate in Cardiac Myocyte

Singh¹,

Adlakha²

2019

Math.Biol.Bioinf.

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Calcium (Ca 2+ ) and inositol 1,4,5-trisphosphate (IP 3 ) is critically important parameters for a vast array of cellular functions. One of the main functions is communication in all parts of the body which is achieved through cell signaling. Abnormalities in Ca 2+ signaling have been implicated in clinically important conditions such as heart failure and cardiac arrhythmias. We propose a mathematical model which systematically investigates complex Ca 2+ and IP 3 dynamics in cardiac myocyte. This two dimensional model is based on calcium-induced calcium release via inositol 1,4,5-trisphosphate receptors and includes calcium modulation of IP 3 levels through feedback regulation of degradation and production. Forward-Time Center-Space method has been used to solve the coupled equations. We were able to reproduce the observed oscillatory patterns in Ca 2+ as well as IP 3 signals. The model predicts that calcium-dependent production and degradation of IP 3 is a key mechanism for complex calcium oscillations in cardiac myocyte. The impact and sensitivity of source, leak, diffusion coefficients on both Ca 2+ and IP 3 dynamics have been investigated. The results show that the relationship between Ca 2+ and IP 3 dynamics is nonlinear.

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Modelling mechanism of calcium oscillations in pancreatic acinar cells

Cited by 47 publications

References 113 publications

Finite element model to study two dimensional unsteady state calcium distribution in cardiac myocytes

Finite element model to study two dimensional unsteady state calcium distribution in cardiac myocytes

Nitric oxide mediates stretch-induced Ca2+ oscillation in smooth muscle

Nonlinear Dynamic Modeling of 2-Dimensional Interdependent Calcium and Inositol 1,4,5-Trisphosphate in Cardiac Myocyte

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