scholarly journals A Cellular Automaton Model as a First Model-Based Assessment of Interacting Mechanisms for Insulin Granule Transport in Beta Cells

Cells ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 1487
Author(s):  
Michael Müller ◽  
Mathias Glombek ◽  
Jeldrick Powitz ◽  
Dennis Brüning ◽  
Ingo Rustenbeck
Keyword(s):  
Cellular Automaton ◽  
Beta Cells ◽  
Transport Processes ◽  
Cellular Automaton Model ◽  
Special Role ◽  
Actin Network ◽  
Cell Interior ◽  
Actin Networks ◽  
Insulin Granules ◽  
Secretion Rates

In this paper a first model is derived and applied which describes the transport of insulin granules through the cell interior and at the membrane of a beta cell. A special role is assigned to the actin network, which significantly influences the transport. For this purpose, microscopically measured actin networks are characterized and then further ones are artificially generated. In a Cellular Automaton model, phenomenological laws for granule movement are formulated and implemented. Simulation results are compared with experiments, primarily using TIRF images and secretion rates. In this respect, good similarities are already apparent. The model is a first useful approach to describe complex granule transport processes in beta cells, and offers great potential for future extensions. Furthermore, the model can be used as a tool to validate hypotheses and associated mechanisms regarding their effect on exocytosis or other processes. For this purpose, the source code for the model is provided online.

scholarly journals Glucose but not KCl diminishes submembrane granule turnover in mouse beta-cells

2017 ◽  
Vol 59 (3) ◽  
pp. 311-324 ◽  
Author(s):  
Dennis Brüning ◽  
Kirstin Reckers ◽  
Peter Drain ◽  
Ingo Rustenbeck
Keyword(s):  
Insulin Secretion ◽  
Beta Cells ◽  
Initial Response ◽  
Secretory Response ◽  
Insulin Granules ◽  
Primary Mouse ◽  
Mouse Islets ◽  
Glucose Stimulated Insulin Secretion ◽  
Secretion Rates ◽  
Reversed Order

KCl depolarization is widely used to mimic the depolarization during glucose-stimulated insulin secretion. Consequently, the insulin secretion elicited by KCl is often regarded as the equivalent of the first phase of glucose-induced insulin secretion. Here, the effects of both stimuli were compared by measuring the secretion of perifused mouse islets, the cytosolic Ca2+ concentration of single beta-cells and the mobility of submembrane insulin granules by TIRF microscopy of primary mouse beta-cells. Two cargo-directed granule labels were used namely insulin-EGFP and C-peptide-emGFP. The granule behaviour common to both was used to compare the effect of sequential stimulation with 40 mM KCl and 30 mM glucose and sequential stimulation with the same stimuli in reversed order. At the level of the cell secretory response, the sequential pulse protocol showed marked differences depending on the order of the two stimuli. KCl produced higher maximal secretion rates and diminished the response to the subsequent glucose stimulus, whereas glucose enhanced the response to the subsequent KCl stimulus. At the level of granule behaviour, a difference developed during the first stimulation phase in that the total number of granules, the short-term resident granules and the arriving granules, which are all parameters of granule turnover, were significantly smaller for glucose than for KCl. These differences at both the level of the cell secretory response and granule behaviour in the submembrane space are incompatible with identical initial response mechanisms to KCl and glucose stimulation.

A CELLULAR AUTOMATON MODEL FOR COLLECTIVE MOTION OF MICROORGANISMS

2007 ◽  
Vol 40 (9) ◽  
pp. 161-166
Author(s):  
Yasushi Iwatani ◽  
Koichi Hashimoto ◽  
Yuki Deguchi
Keyword(s):  
Cellular Automaton ◽  
Collective Motion ◽  
Cellular Automaton Model

A New View of Convective-Diffusive Transport Processes in the Arterial Intima

1991 ◽  
Vol 113 (3) ◽  
pp. 314-329 ◽  
Author(s):  
F. Yuan ◽  
S. Chien ◽  
S. Weinbaum
Keyword(s):  
Early Time ◽  
Transport Processes ◽  
Special Role ◽  
Diffusive Transport ◽  
Internal Elastic Lamina ◽  
Time Model ◽  
Feeding Experiments ◽  
Endothelial Surface ◽  
Extracellular Lipid ◽  
Order Of Magnitude

In this paper a new theoretical framework is presented for analyzing the filtration and macromolecular convective-diffusive transport processes in the intimal region of an artery wall with widely dispersed macromolecular cellular leakage sites, as proposed in the leaky junction-cell turnover hypothesis of Weinbaum et al. [11]. In contrast to existing convection-diffusive models, which assume that the transport is either 1-D, or convection is primarily in a direction normal to the endothelial surface, the present model considers for the first time the nonuniform subendothelial pressure field that arises from the different hydraulic resistances of normal and leaky endothelial clefts and the special role of the internal elastic lamina (IEL) in modulating the horizontal transport of macromolecules after they have passed through the leaky clefts of cells that are either in mitosis or demonstrate IgG labeling. The new theory is able to quantitatively explain the growing body of recent experiments in which an unexpectedly rapid early-time growth of the leakage spot has been observed and the longer time asymptotic behavior in which the leakage spot appears to approach an equilibrium diameter. The new theory also predicts the observed doubling in macromolecular permeability between EBA labeled blue and white areas when the frequency of leakage sites is doubled. This frequency for doubling of permeability, however, is an order of magnitude smaller than predicted by the author’s previous model, Tzeghai et al. [10], in which only convection normal to the endothelial surface was considered and the pressure was uniform in the intima. The longer time model predictions are used to explain the time scale for the formation of liposomes [4] in subendothelial tissue matrix in animal feeding experiments where it has been observed that the extracellular lipid concentration rises sharply prior to the entry of monocytes into the intima [45].

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