scholarly journals A Dynamic Model of Cytosolic Calcium Concentration Oscillations in Mast Cells

Mathematics ◽  
2021 ◽  
Vol 9 (18) ◽  
pp. 2322
Author(s):  
Mingzhu Sun ◽  
Yingchen Li ◽  
Wei Yao

In this paper, a dynamic model of cytosolic calcium concentration () oscillations is established for mast cells (MCs). This model includes the cytoplasm (Cyt), endoplasmic reticulum (ER), mitochondria (Mt), and functional region (μd), formed by the ER and Mt, also with channels in these cellular compartments. By this model, we calculate oscillations that are driven by distinct mechanisms at varying (degradation coefficient of inositol 1, 4, 5-trisphosphate, and production coefficient of ), as well as at different distances between the ER and Mt (ER–Mt distance). The model predicts that (i) Mt and μd compartments can reduce the amplitude of oscillations, and cause the ER to release less during oscillations; (ii) with increasing cytosolic concentration (), the amplitude of oscillations increases (from 0.1 μM to several μM), but the frequency decreases; (iii) the frequency of oscillations decreases as the ER–Mt distance increases. What is more, when the ER–Mt distance is greater than 65 nm, the μd compartment has less effect on oscillations. These results suggest that Mt, μd, and can all affect the amplitude and frequency of oscillations, but the mechanism is different. The model provides a comprehensive mechanism for predicting cytosolic concentration oscillations in mast cells, and a theoretical basis for calcium oscillations observed in mast cells, so as to better understand the regulation mechanism of calcium signaling in mast cells.

2002 ◽  
Vol 70 (8) ◽  
pp. 4692-4696 ◽  
Author(s):  
Mee-Kyung Kim ◽  
Seung-Yong Seong ◽  
Ju-Young Seoh ◽  
Tae-Hee Han ◽  
Hyeon-Je Song ◽  
...  

ABSTRACT Orientia tsutsugamushi shows both pro- and antiapoptotic activities in infected vertebrate cells. Apoptosis of THP-1 cells induced by beauvericin was inhibited by O. tsutsugamushi infection. Beauvericin-induced calcium redistribution was significantly reduced and retarded in cells infected with O. tsutsugamushi. Antiapoptotic activities of O. tsutsugamushi in infected cells are most probably due to inhibition of the increase in the cytosolic calcium concentration.


1999 ◽  
Vol 340 (1) ◽  
pp. 291-297 ◽  
Author(s):  
Matthäus M. RIMPLER ◽  
Ursula RAUEN ◽  
Thorsten SCHMIDT ◽  
Tarik MÖRÖY ◽  
Herbert DE GROOT

The oncoprotein Bcl-2 protects cells against apoptosis, but the exact molecular mechanism that underlies this function has not yet been identified. Studying H2O2-induced cell injury in Rat-1 fibroblast cells, we observed that Bcl-2 had a protective effect against the increase in cytosolic calcium concentration and subsequent cell death. Furthermore, overexpression of Bcl-2 resulted in an alteration of cellular glutathione status: the total amount of cellular glutathione was increased by about 60% and the redox potential of the cellular glutathione pool was maintained in a more reduced state during H2O2 exposure compared with non-Bcl-2-expressing controls. In our cytotoxicity model, disruption of cellular glutathione homoeostasis closely correlated with the pathological elevation of cytosolic calcium concentration. Stabilization of the glutathione pool by Bcl-2, N-acetylcysteine or glucose delayed the cytosolic calcium increase and subsequent cell death, whereas depletion of glutathione by DL-buthionine-(S,R)-sulphoximine, sensitized Bcl-2-transfected cells towards cytosolic calcium increase and cell death. We therefore suggest that the protection exerted by Bcl-2 against H2O2-induced cytosolic calcium elevation and subsequent cell death is secondary to its effect on the cellular glutathione metabolism.


2008 ◽  
Vol 18 (06) ◽  
pp. 883-912 ◽  
Author(s):  
BOGDAN KAZMIERCZAK ◽  
VITALY VOLPERT

The existence and structural stability of travelling waves of systems of the free cytosolic calcium concentration in the presence of immobile buffers are studied. The proof is carried out by passing to zero with the diffusion coefficients of buffers. Thus, its method is different from Ref. 13 where the existence is proved straightforwardly.


Sign in / Sign up

Export Citation Format

Share Document