Calcium: a regulation system emerges in plant cells

Development ◽  
1987 ◽  
Vol 100 (2) ◽  
pp. 181-184
Author(s):  
S. Gilroy ◽  
D.P. Blowers ◽  
A.J. Trewavas
Keyword(s):  
Plasma Membrane ◽  
Calcium Binding ◽  
Regulation System ◽  
Cytoplasmic Calcium ◽  
Channel Activity ◽  
Cytotoxic Effects ◽  
Membrane Perturbation ◽  
Calcium Cells ◽  
Cellular Control ◽  
Signalling Systems

Calcium occupies a pre-eminent place in the cellular control systems of animals (Campbell, 1983). Because of the cytotoxic effects of calcium, cells pay very particular attention to keeping cytoplasmic calcium levels very much lower than the normal extracellular 10-3 M level; usually it is in the range 10-8 -10-6 M. This is accomplished using a variety of calcium-pumping systems located both in the plasma membrane and organelles and together these operate a very efficient calcium-stat system. But, in addition, cells use the temporary elevation of cytoplasmic calcium to between 10-6 and 10-5 M that may follow plasma membrane perturbation and alteration of calcium channel activity, as signals, eliciting a variety of predetermined responses. The concentration of cytoplasmic calcium is sensed by calcium-binding proteins, most notably calmodulin, and the calcium/calmodulin complex in turn modulates the activity of numerous enzymes and proteins. Calcium is also associated with other signalling systems such as IP3 and cyclic AMP.

FEATURES OF CALCIUM HOMEOSTASIS AND CALCIUM SIGNALING IN NEURONS

Vestnik ◽  
2021 ◽  
pp. 208-214
Author(s):  
Б.К. Кайрат ◽  
С.Т. Тулеуханов ◽  
В.П. Зинченко
Keyword(s):  
Plasma Membrane ◽  
Calcium Signaling ◽  
Calcium Binding ◽  
Intracellular Signaling ◽  
Cell Damage ◽  
Compensatory Mechanisms ◽  
Physiological Processes ◽  
Intracellular Ca ◽  
Ca Ions ◽  
Ca Homeostasis

Ионы Са являются основным мессенджером в регуляции физиологических функций клеток. Внутриклеточном пространстве ионы Ca могут свободно состоянии диффундироваться в различных частях цитоплазмы, в то же время значительное количество Ca в связанном виде накапливается в различных внутриклеточных депо или в составе кальций-связывающих белков. Регуляция физиологических процессов с ионами внутриклеточного Са происходит в диапазоне концентраций 10 М, тогда как концентрация Са во внеклеточном пространстве выше и составляет 10 М, для поддержании градиента концентраций в клетках имеются важные Са транспортирующие системы плазматической мембраны, эндоплазматического ретикулума и митохондрий. В нейронах функционируют внутриклеточные ферменты и белки плазматической мембраны для поддержания Са-гомеостаза и реализации механизмов внутриклеточной сигнализации для обеспечения жизнедеятельности в выживании клеток. Нарушение или гиперактивация одного или нескольких механизмов кальциевой сигнализации может привести к повреждению и гибели нейронов в случае отсутствия компенсаторных механизмов. Ca ions are a key messenger for the regulation of most of the physiological functions of cells. Inside the cell, Ca ions can freely diffuse in various parts of the cytoplasm, but a significant amount of Ca is also bound in various intracellular depots or in the form of calcium-binding proteins. The regulation of physiological processes by intracellular Ca ions occurs in the concentration range of 10 M, and the concentration of Ca in the extracellular space is higher and is 10 M, and to maintain this concentration gradient, cells have Ca-transporting systems of the plasma membrane, endoplasmic reticulum and mitochondria. In neurons, a large number of intracellular enzymes and plasma membrane proteins function to maintain Ca-homeostasis and implement intracellular signaling mechanisms to ensure vital activity in the survival of cells. Violation or hyperactivation of one or more mechanisms of calcium signaling can lead to cell damage and death in the absence of compensatory mechanisms.

scholarly journals Moderate Static Magnetic Field (6 mT)-Induced Lipid Rafts Rearrangement Increases Silver NPs Uptake in Human Lymphocytes

Molecules ◽  
2020 ◽  
Vol 25 (6) ◽  
pp. 1398
Author(s):  
Cristian Vergallo ◽  
Elisa Panzarini ◽  
Bernardetta Anna Tenuzzo ◽  
Stefania Mariano ◽  
Ada Maria Tata ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Lipid Rafts ◽  
Lipid Raft ◽  
Human Lymphocytes ◽  
Peripheral Blood Lymphocytes ◽  
Membrane Lipid ◽  
Membrane Perturbation ◽  
Plasma Membrane Lipid ◽  
Silver Nps ◽  
Surface Ligand

One of the most relevant drawbacks in medicine is the ability of drugs and/or imaging agents to reach cells. Nanotechnology opened new horizons in drug delivery, and silver nanoparticles (AgNPs) represent a promising delivery vehicle for their adjustable size and shape, high-density surface ligand attachment, etc. AgNPs cellular uptake involves different endocytosis mechanisms, including lipid raft-mediated endocytosis. Since static magnetic fields (SMFs) exposure induces plasma membrane perturbation, including the rearrangement of lipid rafts, we investigated whether SMF could increase the amount of AgNPs able to pass the peripheral blood lymphocytes (PBLs) plasma membrane. To this purpose, the effect of 6-mT SMF exposure on the redistribution of two main lipid raft components (i.e., disialoganglioside GD3, cholesterol) and on AgNPs uptake efficiency was investigated. Results showed that 6 mT SMF: (i) induces a time-dependent GD3 and cholesterol redistribution in plasma membrane lipid rafts and modulates gene expression of ATP-binding cassette transporter A1 (ABCA1), (ii) increases reactive oxygen species (ROS) production and lipid peroxidation, (iii) does not induce cell death and (iv) induces lipid rafts rearrangement, that, in turn, favors the uptake of AgNPs. Thus, it derives that SMF exposure could be exploited to enhance the internalization of NPs-loaded therapeutic or diagnostic molecules.

Abnormal Calcium Handling by Isolated Cardiac Plasma Membrane from Spontaneously Hypertensive Rats

1981 ◽  
Vol 61 (s7) ◽  
pp. 45s-48s ◽  
Author(s):  
Marie-Gabrielle Pernollet ◽  
Marie-Aude Devynck ◽  
P. Meyer
Keyword(s):  
Plasma Membrane ◽  
Calcium Binding ◽  
Spontaneously Hypertensive Rats ◽  
Membrane Vesicles ◽  
Calcium Handling ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto ◽  
Calcium Extrusion ◽  
Sarcolemmal Vesicles

1. Calcium handling by heart sarcolemmal vesicles from young spontaneously hypertensive rats (SHR) and normotensive Wistar—Kyoto (WKY) control rats were compared. 2. Calcium binding was significantly altered in SHR membranes at the physiological cytosolic Ca2+ concentrations which occur in resting and excited cells. 3. ATP-dependent calcium accumulation occurred at a higher rate in SHR than in WKY rat membrane vesicles. 4. Na+-dependent calcium extrusion of loaded vesicles was higher in SHR than in WKY rat membrane vesicles. 5. These alterations may play a significant role in the pathogenesis of hypertension.

Calsyntenin-1, a Proteolytically Processed Postsynaptic Membrane Protein with a Cytoplasmic Calcium-Binding Domain

2001 ◽  
Vol 17 (1) ◽  
pp. 151-166 ◽  
Author(s):  
Lorenz Vogt ◽  
Sabine P. Schrimpf ◽  
Virginia Meskenaite ◽  
Renato Frischknecht ◽  
Jochen Kinter ◽  
...  
Keyword(s):  
Membrane Protein ◽  
Calcium Binding ◽  
Postsynaptic Membrane ◽  
Binding Domain ◽  
Cytoplasmic Calcium ◽  
Calcium Binding Domain

scholarly journals Estradiol activates epithelial sodium channels in rat alveolar cells through the G protein-coupled estrogen receptor

2013 ◽  
Vol 305 (11) ◽  
pp. L878-L889 ◽  
Author(s):  
Megan M. Greenlee ◽  
Jeremiah D. Mitzelfelt ◽  
Ling Yu ◽  
Qiang Yue ◽  
Billie Jeanne Duke ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Plasma Membrane ◽  
G Protein ◽  
Sodium Channels ◽  
Female Rats ◽  
Channel Activity ◽  
Alveolar Cells ◽  
Α Subunit ◽  
Female Sex ◽  
G Protein Coupled

Female sex predisposes individuals to poorer outcomes during respiratory disorders like cystic fibrosis and influenza-associated pneumonia. A common link between these disorders is dysregulation of alveolar fluid clearance via disruption of epithelial sodium channel (ENaC) activity. Recent evidence suggests that female sex hormones directly regulate expression and activity of alveolar ENaC. In our study, we identified the mechanism by which estradiol (E2) or progesterone (P4) independently regulates alveolar ENaC. Using cell-attached patch clamp, we measured ENaC single-channel activity in a rat alveolar cell line (L2) in response to overnight exposure to either E2 or P4. In contrast to P4, E2 increased ENaC channel activity ( NPo) through an increase in channel open probability ( Po) and an increased number of patches with observable channel activity. Apical plasma membrane abundance of the ENaC α-subunit (αENaC) more than doubled in response to E2 as determined by cell surface biotinylation. αENaC membrane abundance was approximately threefold greater in lungs from female rats in proestrus, when serum E2 is greatest, compared with diestrus, when it is lowest. Our results also revealed a significant role for the G protein-coupled estrogen receptor (Gper) to mediate E2's effects on ENaC. Overall, our results demonstrate that E2 signaling through Gper selectively activates alveolar ENaC through an effect on channel gating and channel density, the latter via greater trafficking of channels to the plasma membrane. The results presented herein implicate E2-mediated regulation of alveolar sodium channels in the sex differences observed in the pathogenesis of several pulmonary diseases.

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