scholarly journals Spatial Relationship and Functional Relevance of Three Lipid Domain Populations at the Erythrocyte Surface

2018 ◽  
Vol 51 (4) ◽  
pp. 1544-1565 ◽  
Author(s):  
Louise Conrard ◽  
Amaury Stommen ◽  
Anne-Sophie Cloos ◽  
Jan Steinkühler ◽  
Rumiana Dimova ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Calcium Influx ◽  
Spatial Relationship ◽  
Calcium Balance ◽  
Lipid Domains ◽  
Calcium Efflux ◽  
Lipid Domain ◽  
Erythrocyte Surface ◽  
Shape Restoration ◽  
Functional Relevance

Background/Aims: Red blood cells (RBC) have been shown to exhibit stable submicrometric lipid domains enriched in cholesterol (chol), sphingomyelin (SM), phosphatidylcholine (PC) or ganglioside GM1, which represent the four main lipid classes of their outer plasma membrane leaflet. However, whether those lipid domains co-exist at the RBC surface or are spatially related and whether and how they are subjected to reorganization upon RBC deformation are not known. Methods: Using fluorescence and/or confocal microscopy and well-validated probes, we compared these four lipid-enriched domains for their abundance, curvature association, lipid order, temperature dependence, spatial dissociation and sensitivity to RBC mechanical stimulation. Results: Our data suggest that three populations of lipid domains with decreasing abundance coexist at the RBC surface: (i) chol-enriched ones, associated with RBC high curvature areas; (ii) GM1/PC/chol-enriched ones, present in low curvature areas; and (iii) SM/PC/chol-enriched ones, also found in low curvature areas. Whereas chol-enriched domains gather in increased curvature areas upon RBC deformation, low curvature-associated lipid domains increase in abundance either upon calcium influx during RBC deformation (GM1/PC/chol-enriched domains) or upon secondary calcium efflux during RBC shape restoration (SM/PC/chol-enriched domains). Hence, abrogation of these two domain populations is accompanied by a strong impairment of the intracellular calcium balance. Conclusion: Lipid domains could contribute to calcium influx and efflux by controlling the membrane distribution and/or the activity of the mechano-activated ion channel Piezo1 and the calcium pump PMCA. Whether this results from lipid domain biophysical properties, the strength of their anchorage to the underlying cytoskeleton and/or their correspondence with inner plasma membrane leaflet lipids remains to be demonstrated.

scholarly journals Spatial Relationship and Functional Relevance of Three Lipid Domain Populations at the Erythrocyte Surface

2019 ◽  
Vol 116 (3) ◽  
pp. 216a
Author(s):  
Louise Conrard ◽  
Amaury Stommen ◽  
Hélène Pollet ◽  
Donatienne Tyteca
Keyword(s):  
Spatial Relationship ◽  
Lipid Domain ◽  
Erythrocyte Surface ◽  
Functional Relevance

scholarly journals Econazole inhibits thapsigargin-induced platelet calcium influx by mechanisms other than cytochrome P-450 inhibition

1993 ◽  
Vol 295 (2) ◽  
pp. 525-529 ◽  
Author(s):  
J G Vostal ◽  
J C Fratantoni
Keyword(s):  
Plasma Membrane ◽  
Antifungal Agents ◽  
Calcium Influx ◽  
Calcium Stores ◽  
Alternative Mechanism ◽  
Resting Cells ◽  
Calcium Efflux ◽  
Plasma Membrane Permeability ◽  
Cytochrome P 450 ◽  
Internal Calcium

Cytochrome P-450 has been suggested as a mediator of the signal between depleted platelet calcium stores and an increase in plasma membrane permeability to calcium which follows depletion of the stores. This hypothesis is based on the observations that inhibitors of cytochrome P-450, such as the imidazole antifungal agents, also inhibit influx of a calcium surrogate (manganese) into calcium-depleted platelets. We tested the effects of econazole and of a cytochrome P-450 inhibitor, carbon monoxide (CO), on thapsigargin (TG)-induced platelet 45Ca2+ influx. TG specifically depletes internal calcium stores and activates store-regulated calcium influx. Econazole blocked 45Ca2+ influx when it was added before TG (IC50 11 microM). Econazole at a concentration (20 microM) that inhibited 83% of TG-induced calcium influx was not inhibitory to TG-induced calcium efflux from 45Ca(2+)-loaded platelets, and did not affect calcium fluxes in resting platelets. This econazole concentration was also inhibitory to calcium influx even when it was added after the stores had been calcium-depleted by EGTA and TG for 15 min and the signal to increase calcium influx had already been generated. Inhibition of cytochrome P-450 with CO bubbled through platelet suspensions did not change calcium influx in resting cells and potentiated TG-induced calcium influx (160% of control calcium accumulation at 20 min). This effect appeared to be concentration-dependent, such that a 5 min exposure to CO produced a greater influx potentiation than a 3 min exposure. These observations indicate that (1) cytochrome P-450 does not mediate store-regulated calcium influx, and (2) econazole probably inhibits store-regulated calcium influx by an alternative mechanism, such as interaction with plasma membrane calcium channels.

scholarly journals Calcitropic effects of recombinant prolactins in Oreochromis mossambicus

1994 ◽  
Vol 266 (4) ◽  
pp. R1302-R1308 ◽  
Author(s):  
G. Flik ◽  
F. Rentier-Delrue ◽  
S. E. Wendelaar Bonga
Keyword(s):  
Plasma Membrane ◽  
Dose Response ◽  
Calcium Influx ◽  
Oreochromis Mossambicus ◽  
Membrane Preparation ◽  
Calcium Efflux ◽  
Branchial Epithelium ◽  
Plasma Membrane Preparation

Homologous recombinant tilapia prolactin-188 (PRL-I) and tilapia prolactin-177 (PRL-II) were tested for calcitropic activity in tilapia, Oreochromis mossambicus. Injection of PRL-I and PRL-II (4 injections, 12.5 pmol/g, over an 8-day period) induced hypercalcemia that resulted from an enhanced calcium influx via the gills and a decreased calcium efflux. Both PRLs increased the density of the Ca(2+)-transporting Ca(2+)-adenosinetriphosphatase in a plasma membrane preparation of the branchial epithelium. Dose-response studies (doses tested: 0.75-12.5 pmol/g) demonstrated that PRL-I was roughly twofold more potent than PRL-II in inducing hypercalcemia, in enhancing basal levels of cortisol, and in stimulating opercular ionocyte density. PRL-I and PRL-II were equipotent in stimulating the dermal mucocyte frequency. We conclude that in this species PRL-I and PRL-II have calcitropic effects, and that PRL-I is more potent than PRL-II in this respect. We postulate that PRL has corticotrophic activity in this fish.

scholarly journals Theoretical Study of the Function of the IP3 Receptor / BK Channel Complex in a Single Neuron

2021 ◽  
Author(s):  
◽  
M. E. Pérez-Bonilla
Keyword(s):  
Plasma Membrane ◽  
Calcium Influx ◽  
Ryanodine Receptors ◽  
Cytosolic Calcium ◽  
Bk Channels ◽  
Bk Channel ◽  
Ip3 Receptors ◽  
Ip3 Receptor ◽  
Calcium Efflux ◽  
The Central Nervous System

Large conductance calcium-activated potassium (BK) channels carry out many functions in the central nervous system. The opening of BK channels requires a rise in the cytosolic calcium ([Ca2+]cyt) concentration, which can occur in two ways: calcium influx from voltage-gated calcium channels (VGCCs) located on the plasma membrane and calcium efflux through the endoplasmic reticulum (ER) membrane to the cytosol triggered by inositol 1,4,5-trisphosphate (IP3) receptors (IP3-Rs) and ryanodine receptors (RyRs). The BK channel/IP3-R/RyR interaction has been widely reported in smooth muscle but scarce information exist on neurons, where its presence is uncertain. The aim of this study was to develop a computational model of a neuron to replicate the interaction between the release of Ca2+ from the ER (through IP3-Rs and RyRs) and the opening of BK channels on the plasma membrane to regulate the level of [Ca2+]cyt, based on the Hodgkin-Huxley formalism and the Goldbeter model. The mathematical models were implemented on Visual Basic® and differential equations were solved numerically. Various conditions of BK conductance and the efflux of endoplasmic Ca2+ were explored. The results show that an abrupt increase in [Ca2+]cyt (≥ 5 mM) activates the BK channels and either pauses or stops the action potential train.

184 INHIBITION OF CALCIUM EFFLUX EXTENDS THE DURATION OF CALCIUM SIGNALS IN PIG OOCYTES

2012 ◽  
Vol 24 (1) ◽  
pp. 204
Author(s):  
L. Y. Yan ◽  
C. Wang ◽  
H. L. Luo ◽  
Z. Machaty
Keyword(s):  
Plasma Membrane ◽  
Intracellular Calcium ◽  
Calcium Influx ◽  
Control Group ◽  
Calcium Signal ◽  
Free Calcium ◽  
Cytoplasmic Calcium ◽  
Free Medium ◽  
Calcium Efflux ◽  
Calcium Signals

Calcium signaling involves the transient elevation in the intracellular free-calcium concentration, which is responsible for controlling a great number of biological functions. In many cell types, a signal is generated when calcium stored in the endoplasmic reticulum is released into the cytoplasm, followed by an influx of calcium across the plasma membrane. At the same time, calcium is removed from the cytosol by ATPases, which pump it back into the intracellular store or out of the cell. The size of the calcium signal is thus determined by the amount of calcium moving into and out of the cytoplasm. In the present study, we investigated the effect of inhibiting the movement of calcium across the plasma membrane on a calcium-signal that was artificially induced in pig oocytes. In vitro-matured pig oocytes were loaded with the calcium-indicator dye, fura-2. The release of calcium from the cytoplasmic stores was stimulated by adding ethanol at a final concentration of 7% and changes in the intracellular free-calcium levels were monitored by using InCyt Im2, a dual-wavelength fluorescence imaging system. In the control group, fluorescent measurements were performed in the presence of extracellular calcium. In additional treatment groups, the ethanol treatment was performed in (1) a calcium-free medium (prevents calcium influx); (2) the presence of 1 mM gadolinium (limits calcium fluxes across the plasma membrane in both directions); and (3) the presence of gadolinium in a calcium-free medium. In each group, 15 oocytes were measured; the data were subjected to 1-way ANOVA and differences between treatment means were compared by the Tukey's test. We found that in control oocytes, 7% ethanol induced a rise of 722.1 ± 49.2 nM in the cytoplasmic calcium levels and the average duration of the calcium transient was 309.1 ± 11.3 s. In the calcium-free medium, this increase was significantly smaller (only 117.9 ± 4.8 nM; P < 0.01), probably because the calcium release was not followed by an influx of calcium across the plasma membrane. In the presence of 1 mM gadolinium in the regular calcium-containing medium, the intracellular calcium levels climbed by 278.8 ± 45.4 nM and dropped to baseline levels only after 773.3 ± 79.9 s. Finally, in the calcium-free medium and in the presence of 1 mM gadolinium, 7% ethanol induced only a small rise (64.5 ± 6.3 nM) in the cytoplasmic calcium levels. These latter increases were both significantly lower (P < 0.01) compared to that in the control group. The results indicate that (1) intracellular calcium signals are sustained by a calcium influx from the extracellular medium and (2) preventing calcium efflux extends the duration of the cytoplasmic calcium elevation in the oocyte. This may have relevance in the manipulation of intracellular calcium levels in oocytes for the development of novel parthenogenetic activation methods.

Calcium efflux of plasma membrane vesicles exposed to ELF magnetic fields-test of a nuclear magnetic resonance interaction model

2012 ◽  
Vol 33 (7) ◽  
pp. 535-542 ◽  
Author(s):  
Wenjun J. Sun ◽  
Mehri Kaviani Mogadam ◽  
Marianne Sommarin ◽  
Henrietta Nittby ◽  
Leif G. Salford ◽  
...  
Keyword(s):  
Nuclear Magnetic Resonance ◽  
Plasma Membrane ◽  
Magnetic Resonance ◽  
Magnetic Fields ◽  
Interaction Model ◽  
Membrane Vesicles ◽  
Resonance Interaction ◽  
Calcium Efflux ◽  
Plasma Membrane Vesicles ◽  
Nuclear Magnetic

scholarly journals Plasma membrane integrity in health and disease: significance and therapeutic potential

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Catarina Dias ◽  
Jesper Nylandsted
Keyword(s):  
Plasma Membrane ◽  
Therapeutic Potential ◽  
Calcium Influx ◽  
Membrane Integrity ◽  
Cell Types ◽  
Physical Parameters ◽  
Membrane Repair ◽  
Plasma Membrane Integrity ◽  
Repair Mechanisms ◽  
And Function

AbstractMaintenance of plasma membrane integrity is essential for normal cell viability and function. Thus, robust membrane repair mechanisms have evolved to counteract the eminent threat of a torn plasma membrane. Different repair mechanisms and the bio-physical parameters required for efficient repair are now emerging from different research groups. However, less is known about when these mechanisms come into play. This review focuses on the existence of membrane disruptions and repair mechanisms in both physiological and pathological conditions, and across multiple cell types, albeit to different degrees. Fundamentally, irrespective of the source of membrane disruption, aberrant calcium influx is the common stimulus that activates the membrane repair response. Inadequate repair responses can tip the balance between physiology and pathology, highlighting the significance of plasma membrane integrity. For example, an over-activated repair response can promote cancer invasion, while the inability to efficiently repair membrane can drive neurodegeneration and muscular dystrophies. The interdisciplinary view explored here emphasises the widespread potential of targeting plasma membrane repair mechanisms for therapeutic purposes.

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