共查询到20条相似文献,搜索用时 31 毫秒
1.
Arachiche A Badirou I Dachary-Prigent J Garcin I Geldwerth-Feniger D Kerbiriou-Nabias D 《Cellular and molecular life sciences : CMLS》2008,65(23):3861-3871
Rapid Ca2+-dependent phospholipid (PL) reorganization (scrambling) at the plasma membrane is a mechanism common to hematopoietic cells
exposing procoagulant phosphatidylserine (PS). The aim of this research was to determine whether activation of the extracellular
signal-regulated kinase (ERK) pathway was required for PL scrambling, based on a single report analyzing both responses induced
by Ca2+ ionophores in megakaryoblastic HEL cells. Ca2+ ionophore-stimulated ERK phosphorylation was induced in platelets without external Ca2+, whereas exogenous Ca2+ entry was crucial for ERK activation in Jurkat T cells. In both cells, membrane scrambling only occurred following Ca2+ entry and was not blocked by inhibiting ERK phosphorylation. Furthermore, ERK proteins are strongly phosphorylated in transformed
B lymphoblastic cell lines, which do not expose PS in their resting state. Overall, the data demonstrated that ERK activation
and membrane scrambling are independent mechanisms.
A. Arachiche, I. Badirou: These authors contributed equally to this work.
Received 18 June 2008; received after revision 24 September 2008; accepted 1 October 2008 相似文献
2.
D. Parolini M. Meregalli M. Belicchi P. Razini R. Lopa B. Del Carlo A. Farini S. Maciotta N. Bresolin L. Porretti M. Pellegrino Y. Torrente 《Cellular and molecular life sciences : CMLS》2009,66(4):697-710
Among the heterogeneous population of circulating hematopoietic and endothelial progenitors, we identified a subpopulation
of CD133+ cells displaying myogenic properties. Unexpectedly, we observed the expression of the B-cell marker CD20 in blood-derived
CD133+ stem cells. The CD20 antigen plays a role in the modulation of intracellular calcium homeostasis through signaling pathways
activation. Several observations suggest that an increase in intracellular calcium concentration ([Ca2+]i) could be involved in the etiology of the Duchenne muscular dystrophy (DMD). Here, we show that a CD20-related signaling
pathway able to induce an increase in [Ca2+]i is differently activated after brain derived neurotrophic factor (BDNF) stimulation of normal and dystrophic blood-derived
CD133+ stem cells, supporting the assumption of a “CD20-related calcium impairment-affecting dystrophic cells. Presented findings
represent the starting point toward the expansion of knowledge on pathways involved in the pathology of DMD and in the behavior
of dystrophic blood-derived CD133+ stem cells.
Received 15 October 2008; received after revision 27 November 2008; accepted 05 December 2008 相似文献
3.
Large conductance, Ca2+-activated potassium (BK) channels are widely expressed throughout the animal kingdom and play important roles in many physiological
processes, such as muscle contraction, neural transmission and hearing. These physiological roles derive from the ability
of BK channels to be synergistically activated by membrane voltage, intracellular Ca2+ and other ligands. Similar to voltage-gated K+ channels, BK channels possess a pore-gate domain (S5–S6 transmembrane segments) and a voltage-sensor domain (S1–S4). In addition,
BK channels contain a large cytoplasmic C-terminal domain that serves as the primary ligand sensor. The voltage sensor and
the ligand sensor allosterically control K+ flux through the pore-gate domain in response to various stimuli, thereby linking cellular metabolism and membrane excitability.
This review summarizes the current understanding of these structural domains and their mutual interactions in voltage-, Ca2+ - and Mg2+ -dependent activation of the channel.
Received 25 September 2008; received after revision 23 October 2008; accepted 24 October 2008 相似文献
4.
Proinsulin C-peptide and its analogues induce intracellular Ca2+ increases in human renal tubular cells 总被引:3,自引:0,他引:3
Shafqat J Juntti-Berggren L Zhong Z Ekberg K Köhler M Berggren PO Johansson J Wahren J Jörnvall H 《Cellular and molecular life sciences : CMLS》2002,59(7):1185-1189
Based on the findings that proinsulin C-peptide binds specifically to cell membranes, we investigated the effects of C-peptide
and related molecules on the intracellular Ca2+ concentration ([Ca2+]i) in human renal tubular cells using the indicator fura-2/AM. The results show that human C-peptide and its C-terminal pentapeptide
(positions 27–31, EGSLQ), but not the des (27–31) C-peptide or randomly scrambled C-peptide, elicit a transient increase in
[Ca2+]i. Rat C-peptide and rat C-terminal pentapeptide also induce a [Ca2+]i response in human tubular cells, while a human pentapeptide analogue with Ala at position 1 gives no [Ca2+]i response, and those with Ala at positions 2–5 induce responses with different amplitudes. These results define a species
cross-reactivity for C-peptide and demonstrate the importance of Glu at position 1 of the pentapeptide. Preincubation of cells
with pertussis toxin abolishes the effect on [Ca2+]i by both C-peptide and the pentapeptide. These results are compatible with previous data on C-peptide binding to cells and
activation of Na+,K+ATPase. Combined, all data show that C-peptide is a bioactive peptide and suggest that it elicits changes in [Ca2+]i via G-protein-coupled pathways, giving downstream enzyme effects.
Received 13 May 2002; accepted 16 May 2002 相似文献
5.
C. J. Duncan 《Cellular and molecular life sciences : CMLS》1979,35(6):817-818
Summary The actions on amphibian embryos of UV-irradiation, exposure to Li+ or exposure to ouabain show interesting parallels with their effects on spontaneous release at the presynaptic terminals of the neuromuscular junction. It is suggested that these treatments serve to raise intracellular Ca2+ ([Ca2+
i) in these examples, and that UV-promoted abnormalities in embryogenesis are a consequence of changes in [Ca2+]i at critical stages in development. 相似文献
6.
D. Chao G. Balboni L. H. Lazarus S. Salvadori Y. Xia 《Cellular and molecular life sciences : CMLS》2009,66(6):1105-1115
Activation of δ-opioid receptors (DOR) attenuates anoxic K+ leakage and protects cortical neurons from anoxic insults by inhibiting Na+ influx. It is unknown, however, which pathway(s) that mediates the Na+ influx is the target of DOR signal. In the present work, we found that, in the cortex, (1) DOR protection was largely dependent
on the inhibition of anoxic Na+ influxes mediated by voltage-gated Na+ channels; (2) DOR activation inhibited Na+ influx mediated by ionotropic glutamate N-methyl-D-aspartate (NMDA) receptors, but not that by non-NMDA receptors, although both played a role in anoxic K+ derangement; and (3) DOR activation had little effect on Na+/Ca2+ exchanger-based response to anoxia. We conclude that DOR activation attenuates anoxic K+ derangement by restricting Na+ influx mediated by Na+ channels and NMDA receptors, and that non-NMDA receptors and Na+/Ca2+ exchangers, although involved in anoxic K+ derangement in certain degrees, are less likely the targets of DOR signal.
Received 26 November 2008; received after revision 26 December 2008; accepted 13 January 2009 相似文献
7.
Wang SH Shih YL Ko WC Wei YH Shih CM 《Cellular and molecular life sciences : CMLS》2008,65(22):3640-3652
The cytotoxicity of cadmium (Cd) induced autophagy and apoptosis in MES-13 cells was determined by flow cytometry. Autophagy
was also assessed by formation of autophagosomes and processing of LC3. Pharmacological inhibition of autophagy resulted in
increased of cell viability, suggesting autophagy plays a role in cell death in Cd-treated mesangial cells. Cd also induced
a rapid elevation in cytosolic calcium ([Ca2+]i ), and modulation of [Ca2+]i via treatment with IP
3R inhibitor or knockdown of calcineurin resulted in a change in the proportion of cell death, suggesting that the release
of calcium from the ER plays a crucial role in Cd-induced cell death. Inhibition of Cd-induced ERK activation by PD 98059
suppressed Cd-induced autophagy, and BAPTA-AM eliminated activation of ERK. BAPTA-AM also inhibited Cd-induced mitochondrial
depolarization and activation of caspases. These findings demonstrated that Cd induces both autophagy and apoptosis through
elevation of [Ca2+]i, followed by Ca2+-ERK and Ca2+-mitochondria-caspase signaling pathways.
Electronic supplementary material The online version of this article (doi:) contains supplementary material, which is available to authorized users.
Received 05 July 2008; received after revision 25 August 2008; accepted 17 September 2008 相似文献
8.
Summary The role of Ca2+ in secretagogue-induced insulin release is documented not only by the measurements of45Ca fluxes in pancreatic islets, but also, by direct monitoring of cytosolic free Ca2+, [Ca2+]i. As demonstrated, using the fluorescent indicator quin 2, glyceraldehyde, carbamylcholine and alanine raise [Ca2+]i in the insulin secreting cell line RINm5F, whereas glucose has a similar effect in pancreatic islet cells. The regulation of cellular Ca2+ homeostasis by organelles from a rat insulinoma, was investigated with a Ca2+ selective electrode. The results suggest that both the endoplasmic reticulum and the mitochondria participate in this regulation, albeit at different Ca2+ concentrations. By contrast, the secretory granules do not appear to be involved in the short-term regulation of [Ca2+]i. Evidence is presented that inositol 1,4,5-trisphosphate, which is shown to mobilize Ca2+ from the endoplasmic reticulum, is acting as an intracellular mediator in the stimulation of insulin release. 相似文献
9.
P. C. Newell D. Malchow J. D. Gross 《Cellular and molecular life sciences : CMLS》1995,51(12):1155-1165
Changes in cytosolic Ca2+ play an important role in a wide array of cell types and the control of its concentration depends upon the interplay of many cellular constituents. Resting cells maintain cytosolic calcium ([Ca2+]i) at a low level in the face of steep gradients of extracellular and sequestered Ca2+. Many different signals can provoke the opening of calcium channels in the plasma membrane or in intracellular compartments and cause rapid influx of Ca2+ into the cytosol and elevation of [Ca2+]i. After such stimulation Ca2+ ATPases located in the plasma membrane and in the membranes of intracellular stores rapidly return [Ca2+]i to its basal level. Such responses to elevation of [Ca2+]i are a part of an important signal transduction mechanism that uses calcium (often via the binding protein calmodulin) to mediate a variety of cellular actions responsive to outside influences. 相似文献
10.
Using a newly developed microcalorimetric approach to assess the rate of energy expenditure for intracellular [Ca2+] homeostasis in isolated muscles at rest, we found this was lower inmdx than in control mouse muscles, by 62% and 29% in soleus and extensor digitorum longus, respectively. Differences in total and Ca2+-dependent rates of specific heat production betweenmdx and control were enhanced during sustained, KCl-induced stimulation of energy dissipation. These results suggest that the low sacroplasmic energy status of dystrophic muscles is not due to any excessive energy expenditure for intracellular [Ca2+] homeostasis. 相似文献
11.
Shao-Nian Yang Yue Shi Guang Yang Yuxin Li Jia Yu Per-Olof Berggren 《Cellular and molecular life sciences : CMLS》2014,71(21):4149-4177
The function and survival of pancreatic β cells critically rely on complex electrical signaling systems composed of a series of ionic events, namely fluxes of K+, Na+, Ca2+ and Cl? across the β cell membranes. These electrical signaling systems not only sense events occurring in the extracellular space and intracellular milieu of pancreatic islet cells, but also control different β cell activities, most notably glucose-stimulated insulin secretion. Three major ion fluxes including K+ efflux through ATP-sensitive K+ (KATP) channels, the voltage-gated Ca2+ (CaV) channel-mediated Ca2+ influx and K+ efflux through voltage-gated K+ (KV) channels operate in the β cell. These ion fluxes set the resting membrane potential and the shape, rate and pattern of firing of action potentials under different metabolic conditions. The KATP channel-mediated K+ efflux determines the resting membrane potential and keeps the excitability of the β cell at low levels. Ca2+ influx through CaV1 channels, a major type of β cell CaV channels, causes the upstroke or depolarization phase of the action potential and regulates a wide range of β cell functions including the most elementary β cell function, insulin secretion. K+ efflux mediated by KV2.1 delayed rectifier K+ channels, a predominant form of β cell KV channels, brings about the downstroke or repolarization phase of the action potential, which acts as a brake for insulin secretion owing to shutting down the CaV channel-mediated Ca2+ entry. These three ion channel-mediated ion fluxes are the most important ionic events in β cell signaling. This review concisely discusses various ionic mechanisms in β cell signaling and highlights KATP channel-, CaV1 channel- and KV2.1 channel-mediated ion fluxes. 相似文献
12.
C. J. Duncan 《Cellular and molecular life sciences : CMLS》1977,33(7):923-924
Summary It is suggested that ouabain promotes catecholamine release by causing a rise in intracellular Na+ which, in turn, causes an elevated steady-state level of intracellular Ca2+. It is suggested that the Na+–K+-ATPase is not directly involved in exocytosis at either adrenergic or cholinergic synapses. 相似文献
13.
P. Y. D. Wong 《Cellular and molecular life sciences : CMLS》1980,36(5):570-571
Summary Intracellular potentials in the cells from 17.5-day old rat visceral yolk sacs were measured by a glass microelectrode. When penetrated from the maternal side, the cells have potentials of about 50.2±1.9 mV (inside negative) which were reduced by increasing the external K+ concentration and increased by removing Na+ ions from the bathing fluid. Triaminopyrimidine (TAP) which inhibited Na+ transport caused a dose-dependent depolarization of the cell membrane. The depolarization was dependent on the presence of extracellular Ca2+ ions. It is proposed that TAP may inhibit Na+ transport by increasing the intracellular concentration of calcium ions.This work was supported by the University of Hong Kong (grant number 335. 034.5105).Acknowledgment. Triaminopyrimidine was synthesized by Dr. Barbara Roth of the Wellcome Research Laboratories. 相似文献
14.
S. Weidmann 《Cellular and molecular life sciences : CMLS》1987,43(2):133-146
Summary The time-course of the cardiac action potential can be accounted for in terms of ionic currents crossing the cell membranes. Depolarizing current is carried by Na+ or Ca2+ entering the cells, repolarizing current by K+ leaving the cells. Membrane permeability for the passive movement of these ions is thought to be voltage-dependent as well as time-dependent. Net transfer of charge may also result from active transport, 2 Na+ out against 1 K+ in; or coupled exchange, 3 or 4 Na+ in against 1 Ca2+ out. This review follows the path by which present-day knowledge has been reached. It also gives a few examples to illustrate that electrophysiology has provided concepts useful to clinical cardiology. 相似文献
15.
Summary Morphine inhibited the noradrenaline release from slices of rat brain cortex induced by introduction of Ca2+ ions after superfusion with Ca2+-free, K+-rich solution. The degree of inhibition was inversely related to the Ca2+ concentration used for stimulation.Acknowledgment. We thank Mrs G. Thielecke and Miss G. Werthmann for technical assistance. 相似文献
16.
T. Nasu 《Cellular and molecular life sciences : CMLS》1993,49(10):865-869
Preincubation with 0.3 mM Zn2+ markedly inhibited both the tonic response and Ca2+ binding at low affinity sites induced by K+ (60 mM), with smaller effects on the phasic response and the high affinity Ca2+ sites, inTaenia coli. However, when the muscle was kept in Zn2+-containing medium following the first stimulation with the K+, the phasic response and the high affinity Ca2+ sites were more severely inhibited during the second stimulation with K+. This probably indicates that Zn2+ reduced the tonic tension response to K+ mainly by inhibiting Ca2+ influx at the cell membranes ofTaenia coli. However, when Zn2+ is continuously present, Ca2+ is not supplied at the storage sites and is not available for the phasic response to a second stimulation with K+. 相似文献
17.
F. Wuytack L. Raeymaekers R. Casteels 《Cellular and molecular life sciences : CMLS》1985,41(7):900-905
Summary A calmodulin stimulated Ca2+-transport ATPase which has many of the characteristics of the erythrocyte type Ca2+-transport ATPase has been purified from smooth muscle. In particular, the effect of calmodulin on these transport enzymes is mimiced by partial proteolysis and antibodies against erythrocyte Ca2+-transport ATPase also bind to the smooth muscle (Ca2++Mg2+)ATPase. A correlation between the distribution of the calmodulin stimulated (Ca2++Mg2+)ATPase and (Na++K+)ATPase activities in smooth muscle membranes separated by density gradient centrifugation suggests a plasmalemmal distribution of this (Ca2++Mg2+)ATPase. A phosphoprotein intermediate in smooth muscle which strongly resembles the corresponding phosphoprotein in sarcoplasmic reticulum of skeletal muscle may indicate the presence in smooth muscle of a similar type of Ca2+-transport ATPase. 相似文献
18.
The effect of a phorbol ester upon the cholinergic regulation of potassium permeability in the rat submandibular gland 总被引:1,自引:0,他引:1
Acetylcholine releases calcium from cytoplasmic stores and permits an influx of calcium in salivary acinar cells. The resultant rise in [Ca2+]i causes an increase in potassium permeability which is an important part of the secretory response. We have investigated the effects of 12-0-tetradecanoyl phorbol-13-acetate, a potent activator of protein kinase C, upon this regulation of potassium permeability in superfused pieces of rat submandibular salivary gland. This compound inhibited the initial [Ca2+]o-independent component of the response of acetylcholine but had no effect upon the subsequent [Ca2+]o-dependent phase. This compound does not, therefore, appear to inhibit receptor-regulated calcium influx. 相似文献
19.
Sampaio MS Bezerra IP Peçanha FL Fonseca PH Capella MA Lopes AG 《Cellular and molecular life sciences : CMLS》2008,65(19):3093-3099
The lack of Na+,K+-ATPase expression in intercalated cells (IC) is an intriguing condition due to its fundamental role in cellular homeostasis.
In order to better understand this question we compared the activities of Na+,K+-ATPase and Na+-ATPase in two MDCK cell clones: the C11, with IC characteristics, and the C7, with principal cells (PC) characteristics.
The Na+,K+-ATPase activity found in C11 cells is far lower than in C7 cells and the expression of its β-subunit is similar in both cells.
On the other hand, a subset of C11 without α-subunit expression has been found. In C11 cells the Na+-ATPase activity is higher than that of the Na+,K+-ATPase, and it is increased by medium alkalinization, suggesting that it could account for the cellular Na+-homeostasis. Although further studies are necessary for a better understanding of these findings, the presence of Na+-ATPase may explain the adequate survival of cells that lack Na+,K+-ATPase.
Received 09 July 2008; received after revision 03 August 2008; accepted 12 August 2008 相似文献
20.
J. Diez P. Braquet R. Verna C. Nazaret R. P. Garay 《Cellular and molecular life sciences : CMLS》1985,41(5):666-667
Summary Exogenous cyclic AMP (cAMP) inhibits the Na+, K+-cotransport system and stimulates the Na+, K+-pump and Na+, Ca2+ exchange in mouse macrophages. These effects are enhanced by inhibition of phosphodiesterase with methylisobutylxanthine (MIX). MIX alone showed little or no effect. A similar response was observed after stimulation of endogenous production of cAMP by isoproterenol. 相似文献