Sevoflurane but not propofol provided dual effects of cell survival in human neuroblastoma SH-SY5Y cells

2021 ◽  
Vol 18 ◽  
Author(s):  
Xue Gao ◽  
Xiu Wang ◽  
Lei Zhang ◽  
Ge Liang ◽  
Rachel Mund ◽  
...  
Keyword(s):  
Cell Survival ◽  
Prolonged Exposure ◽  
Calcium Influx ◽  
Cell Damage ◽  
Cytosolic Calcium ◽  
Extracellular Calcium ◽  
Mitochondrial Calcium ◽  
General Anesthetics ◽  
Wild Type ◽  
Human Neuroblastoma

Background: We have hypothesized that the most commonly used intravenous (propofol) and inhalational (sevoflurane) general anesthetics affect cell survival concentration and duration dependently with different potency associated with their differential potency to affect intracellular calcium homeostasis. Methods: Human neuroblastoma SH-SY5Y cells stably transfected with either wild type or M146L mutant human presenilin 1 were cultured and exposed to equipotent of propofol or sevoflurane. Cell viability, cytosolic and mitochondrial calcium were measured. Results: Sevoflurane but not propofol, at clinically relevant concentrations and durations, promoted cell survival. Prolonged exposure (24 hours) of 1% sevoflurane resulted in significant cell damage in both types of cells. Both sevoflurane and propofol had significantly higher cell response rates to the elevation of cytosolic calcium or mitochondrial calcium in the presence of extracellular calcium. With the contribution of calcium influx, sevoflurane but not equipotent 1 MAC propofol, caused a significantly greater increase in peak and overall calcium in Alzheimer’s mutation cell than in wild type cells, but significantly more increase in overall mitochondrial calcium concentrations in wild type than mutation cells. In the absence of extracellular calcium influx, sevoflurane, but not propofol, caused more significant elevations of overall mitochondrial calcium concentration in mutation cells than control cells. Conclusion: Calcium influx contributed to the general anesthetics mediated elevation of cytosolic or mitochondrial calcium, which is especially true for propofol. Sevoflurane has a greater potency to either promote or inhibit cell survival than propofol, which may be associated with its ability to affect cytosolic or mitochondrial calcium.

Modulation of frequency and height of cytosolic calcium spikes by plasma membrane anion channels in guard cells

2021 ◽  
Author(s):  
Md Tahjib-Ul-Arif ◽  
Shintaro Munemasa ◽  
Toshiyuki Nakamura ◽  
Yoshimasa Nakamura ◽  
Yoshiyuki Murata
Keyword(s):  
Plasma Membrane ◽  
Stomatal Closure ◽  
Anion Channel ◽  
Guard Cells ◽  
Cytosolic Calcium ◽  
Peak Height ◽  
Extracellular Calcium ◽  
Wild Type ◽  
Anion Channels ◽  
In The Wild

Abstract Cytosolic calcium ([Ca2+]cyt) elevation activates plasma membrane anion channels in guard cells, which is required for stomatal closure. However, involvement of the anion channels in the [Ca2+]cyt elevation remains unclear. We investigated the involvement using Arabidopsis thaliana anion channel mutants, slac1-4 slah3-3 and slac1-4 almt12-1. Extracellular calcium induced stomatal closure in the wild-type plants but not in the anion channel mutant plants whereas extracellular calcium induced [Ca2+]cyt elevation both in the wild-type guard cells and in the mutant guard cells. The peak height and the number of the [Ca2+]cyt spike were lower and larger in the slac1-4 slah3-3 than in the wild-type and the height and the number in the slac1-4 almt12-1 were much lower and much larger than in the wild-type. These results suggest that the anion channels are involved in the regulation of [Ca2+]cyt elevation in guard cells.

Effect of osmolality on cytosolic free calcium and aldosterone secretion

1992 ◽  
Vol 262 (1) ◽  
pp. E68-E75 ◽  
Author(s):  
W. Wang ◽  
N. Hayama ◽  
T. V. Robinson ◽  
R. E. Kramer ◽  
E. G. Schneider
Keyword(s):  
Calcium Influx ◽  
Potassium Concentration ◽  
Sodium Concentration ◽  
Cytosolic Calcium ◽  
Extracellular Calcium ◽  
Free Calcium ◽  
Aldosterone Secretion ◽  
Voltage Dependent ◽  
Glomerulosa Cells ◽  
Dose Dependent

Alterations in extracellular osmolality have powerful inverse effects on basal and potassium- and angiotensin-stimulated aldosterone secretion. With the use of bovine glomerulosa cells grown in primary culture, the effects of alterations in osmolality on cytosolic calcium concentration ([Ca2+]c), efflux and uptake of 45Ca2+, and aldosterone secretion were determined. Alterations in osmolality, independent of sodium concentration, have inverse effects on aldosterone secretion, which are correlated with simultaneous changes in [Ca2+]c measured using fura-2. Reductions in osmolality cause dose-dependent biphasic increases in [Ca2+]c different from the monophasic increases in [Ca2+]c produced by increases in potassium concentration. Like potassium- and angiotensin-stimulated increases in [Ca2+]c, hypotonically induced increases in [Ca2+]c are associated with an increase in 45Ca2+ efflux. Reductions in osmolality also increased the uptake of 45Ca2+, an effect apparent at 2 min and persistent for at least 30 min. In the absence of extracellular calcium, reductions in osmolality, as increases in potassium concentration but not angiotensin, fail to increase [Ca2+]c, efflux of 45Ca2+, or aldosterone secretion. In conclusion, osmolality-induced alterations in aldosterone secretion are associated with parallel changes in [Ca2+]c, effects caused by alteration in the influx of extracellular calcium. On the basis of these and previous studies, we hypothesize that osmolality affects calcium influx by activating voltage-dependent or stretch-activated calcium channels.

Extracellular Ca2+ directly regulates tight junctional permeability in the human cervical cell line CaSki

1997 ◽  
Vol 272 (2) ◽  
pp. C511-C524 ◽  
Author(s):  
G. I. Gorodeski ◽  
W. Jin ◽  
U. Hopfer
Keyword(s):  
Tight Junctions ◽  
Calcium Concentration ◽  
Calcium Influx ◽  
Partial Agonist ◽  
Electrical Conductance ◽  
Cytosolic Calcium ◽  
Extracellular Calcium ◽  
Maximal Effect ◽  
Response Curves ◽  
Junctional Permeability

Lowering extracellular calcium concentration ([Ca2+]o) increases acutely and reversibly the transepithelial electrical conductance (G(TE)) and the epithelial permeability to pyranine (Ppyr) across CaSki cultures. Effects were already observed after lowering calcium from 1.2 to 1.0 mM and were maximal at 0.1 mM. The dose-response curves were sigmoidal (calcium concentration that produces half-maximal effect = 0.3 mM), and the time courses indicated simple exponential trends (time constants of 4-5 min). The effect of calcium was not mediated by mobilization of cytosolic calcium or altering calcium influx, and manganese was found to be a partial agonist to [Ca2+]o. The effects of [Ca2+]o, on permeability were additive to those of hypertonic conditions, indicating that calcium modulates junctional permeability. The experimental data were fitted to theoretical models that relate changes in G(TE) to the probability of assembled/disassembled tight junctions. The results suggest that calcium interacts directly and cooperatively at extracellular sites with junctional elements that are arranged in parallel, and it shifts the probability state of the junctions from "open" to "closed" state. Changes in extracellular calcium may affect the permeability of tight junctions of the cervical epithelium and may play a role in regulating production of cervical mucus.

scholarly journals Widely Conserved Attenuation of Plant MAMP-Induced Calcium Influx by Bacteria Depends on Multiple Virulence Factors and May Involve Desensitization of Host Pattern Recognition Receptors

2019 ◽  
Vol 32 (5) ◽  
pp. 608-621 ◽  
Author(s):  
Meltem Lammertz ◽  
Hannah Kuhn ◽  
Sebastian Pfeilmeier ◽  
Jacob Malone ◽  
Cyril Zipfel ◽  
...  
Keyword(s):  
Pattern Recognition ◽  
Immune Responses ◽  
Pseudomonas Syringae ◽  
Prolonged Exposure ◽  
Calcium Influx ◽  
Bacterial Species ◽  
Cytosolic Calcium ◽  
Pattern Recognition Receptors ◽  
Effector Proteins ◽  
Virulence Determinants

Successful pathogens must efficiently defeat or delay host immune responses, including those triggered by release or exposure of microbe-associated molecular patterns (MAMPs). Knowledge of the molecular details leading to this phenomenon in genuine plant–pathogen interactions is still scarce. We took advantage of the well-established Arabidopsis thaliana–Pseudomonas syringae pv. tomato DC3000 pathosystem to explore the molecular prerequisites for the suppression of MAMP-triggered host defense by the bacterial invader. Using a transgenic Arabidopsis line expressing the calcium sensor apoaequorin, we discovered that strain DC3000 colonization results in a complete inhibition of MAMP-induced cytosolic calcium influx, a key event of immediate-early host immune signaling. A range of further plant-associated bacterial species is also able to prevent, either partially or fully, the MAMP-triggered cytosolic calcium pattern. Genetic analysis revealed that this suppressive effect partially relies on the bacterial type III secretion system (T3SS) but cannot be attributed to individual members of the currently known arsenal of strain DC3000 effector proteins. Although the phytotoxin coronatine and bacterial flagellin individually are dispensable for the effective inhibition of MAMP-induced calcium signatures, they contribute to the attenuation of calcium influx in the absence of the T3SS. Our findings suggest that the capacity to interfere with early plant immune responses is a widespread ability among plant-associated bacteria that, at least in strain DC3000, requires the combinatorial effect of multiple virulence determinants. This may also include the desensitization of host pattern recognition receptors by the prolonged exposure to MAMPs during bacterial pathogenesis.

scholarly journals Mitochondrial Calcium Buffering Contributes to the Maintenance of Basal Calcium Levels in Mouse Taste Cells

2008 ◽  
Vol 100 (4) ◽  
pp. 2177-2191 ◽  
Author(s):  
Kyle Hacker ◽  
Kathryn F. Medler
Keyword(s):  
Signaling Pathways ◽  
Calcium Release ◽  
Transient Receptor Potential ◽  
Calcium Influx ◽  
Taste Receptor ◽  
Cell Types ◽  
Cytosolic Calcium ◽  
Mitochondrial Calcium ◽  
Calcium Buffering ◽  
Taste Cells

Taste stimuli are detected by taste receptor cells present in the oral cavity using diverse signaling pathways. Some taste stimuli are detected by G protein–coupled receptors (GPCRs) that cause calcium release from intracellular stores, whereas other stimuli depolarize taste cells to cause calcium influx through voltage-gated calcium channels (VGCCs). Although taste cells use two distinct mechanisms to transmit taste signals, increases in cytosolic calcium are critical for normal responses in both pathways. This creates a need to tightly control intracellular calcium levels in all transducing taste cells. To date, however, the mechanisms used by taste cells to regulate cytosolic calcium levels have not been identified. Studies in other cell types have shown that mitochondria can be important calcium buffers, even during small changes in calcium loads. In this study, we used calcium imaging to characterize the role of mitochondria in buffering calcium levels in taste cells. We discovered that mitochondria make important contributions to the maintenance of resting calcium levels in taste cells by routinely buffering a constitutive calcium influx across the plasma membrane. This is unusual because in other cell types, mitochondrial calcium buffering primarily affects large evoked calcium responses. We also found that the amount of calcium that is buffered by mitochondria varies with the signaling pathways used by the taste cells. A transient receptor potential (TRP) channel, likely TRPV1 or a taste variant of TRPV1, contributes to the constitutive calcium influx.

Pollen Tube Growth and the Intracellular Cytosolic Calcium Gradient Oscillate in Phase while Extracellular Calcium Influx Is Delayed

1997 ◽  
Vol 9 (11) ◽  
pp. 1999 ◽  
Author(s):  
Terena L. Holdaway-Clarke ◽  
Jose A. Feijo ◽  
Grant R. Hackett ◽  
Joseph G. Kunkel ◽  
Peter K. Hepler
Keyword(s):  
Pollen Tube ◽  
Pollen Tube Growth ◽  
Calcium Influx ◽  
Cytosolic Calcium ◽  
Extracellular Calcium ◽  
Tube Growth ◽  
Calcium Gradient

Effect of calcium on transport characteristics of cultured proximal renal cells

1985 ◽  
Vol 249 (3) ◽  
pp. F346-F355
Author(s):  
L. M. Sakhrani ◽  
N. Tessitore ◽  
S. G. Massry
Keyword(s):  
Phosphate Uptake ◽  
Cytosolic Calcium ◽  
Ruthenium Red ◽  
Extracellular Calcium ◽  
Transport Processes ◽  
Renal Cells ◽  
Sodium Uptake ◽  
Calcium Loading ◽  
Sodium Dependent ◽  
Acute Changes

We examined the effects of acute changes in extracellular and intracellular calcium on transport processes in primary culture of proximal rabbit renal cells. A change in extracellular calcium from 0 to 3 mM inhibited amiloride-sensitive sodium uptake by 30%, and this effect was maximal at 1 mM calcium. Other polyvalent cations (Mn2+, Mg2+, La3+, and Ba2+) produced quantitatively similar inhibition of amiloride-sensitive sodium uptake compared with calcium. An increase in cytosolic calcium produced by calcium loading (20 mM) or by A23187 (20 microM) resulted in an inhibition of 25-40% of amiloride-sensitive sodium uptake. Moreover, quinidine (10(-4)M) and ruthenium red (3 microM), agents presumed to increase cytosolic calcium, inhibited amiloride-sensitive sodium uptake by 20-60%. Both these agents also inhibited sodium-dependent phosphate uptake by 20% but had no effect on ouabain-sensitive 86Rb+ uptake or on sodium-dependent alpha-methylglucoside uptake. Our data indicate that increases in extracellular calcium inhibit amiloride-sensitive sodium uptake and increases in cytosolic calcium inhibit sodium-dependent phosphate and amiloride-sensitive sodium uptakes. The effect of extracellular calcium may be due to charge screening and/or binding to the negatively charged plasma membrane or due to alterations in membrane fluidity.

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