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1.
Z. I. Krutetskaya L. S. Milenina A. A. Naumova S. N. Butov V. G. Antonov A. D. Nozdrachev 《Doklady. Biochemistry and biophysics》2018,478(1):44-46
Using Fura-2AM microfluorimetry, we have shown for the first time that preincubation of macrophages with the calsequestrin inhibitor neuroleptic trifluoperazine leads to a significant inhibition of the store-dependent Ca2+ entry induced by endoplasmic Ca2+-ATPase inhibitors thapsigargin or cyclopiazonic acid in rat peritoneal macrophages. The results suggest calsequestrin involvement in the regulation of the store-dependent Ca2+ entry in macrophages. 相似文献
2.
We studied store-dependent (activated by depletion of the endoplasmic reticulum, ER, store) entry of Ca2+ from the extracellular medium into neurons of the rat spinal ganglia (small- and medium-sized cells; diameter, 18 to 36 μm).
Activation of ryanodine-sensitive receptors of the ER in the studied neurons superfused by Tyrode solutions containing Ca2+ or with no Ca2+ was provided by application of 10 mM caffeine. The decay phase of caffeine-induced calcium transients in a Ca2+-containing solution was significantly longer than that in a Ca2+-free solution. This fact allows us to suppose that such a phenomenon is determined by Ca2+ entry into the neuron from the extracellular medium activated by caffeine-induced depletion of the ER store. Substitution
of Ca2+-free extracellular solution by Ca2+-containing Tyrode solution, after depletion of the ER stores induced by applications of 100 nM ryanodine, 200 μM ATP, or
1 μM thapsigargin, resulted in increases in the concentration of intracellular Ca2+. These observations allow us to postulate that store-dependent Ca2+ entry into the studied neurons is activated after depletion not only of the inositol trisphosphate-sensitive ER store but
also of the ryanodine-sensitive store. This entry also occurs after blocking of ATPases of the ER by thapsigargin. The kinetic
characteristics of the rising phase of store-dependent Ca2+ entry induced by depletion of the ER stores under the influence of various agents are dissimilar; this can be related to
different mechanisms of activation of such signals and/or to a compartmental organization of the ER.
Neirofiziologiya/Neurophysiology, Vol. 37, No. 3, pp. 277–283, May–June, 2005. 相似文献
3.
Z. I. Krutetskaya L. S. Milenina A. A. Naumova S. N. Butov V. G. Antonov A. D. Nozdrachev 《Doklady. Biochemistry and biophysics》2018,481(1):222-224
Using Fura-2AM microfluorimetry, we have shown for the first time that sigma-1 receptor agonist, tricyclic antidepressant amitriptyline, significantly inhibits glutoxim- and molixan-induced Ca2+-responses in rat peritoneal macrophages. The results suggest possible involvement of sigma-1 receptors in the signaling cascade induced by glutoxim or molixan and leading to intracellular Ca2+ concentration increase in macrophages. 相似文献
4.
Chen ML Chen YC Peng IW Kang RL Wu MP Cheng PW Shih PY Lu LL Yang CC Pan CY 《Journal of biomedical science》2008,15(2):169-181
Summary Calcium binding protein-1 (CaBP1) is a calmodulin like protein shown to modulate Ca2+ channel activities. Here, we explored the functions of long and short spliced CaBP1 variants (L- and S-CaBP1) in modulating
stimulus-secretion coupling in primary cultured bovine chromaffin cells. L- and S-CaBP1 were cloned from rat brain and fused
with yellow fluorescent protein at the C-terminal. When expressed in chromaffin cells, wild-type L- and S-CaBP1s could be
found in the cytosol, plasma membrane and a perinuclear region; in contrast, the myristoylation-deficient mutants were not
found in the membrane. More than 20 and 70% of Na+ and Ca2+ currents, respectively, were inhibited by wild-type isoforms but not myristoylation-deficient mutants. The [Ca2+]
i
response evoked by high K+ buffer and the exocytosis elicited by membrane depolarizations were inhibited only by wild-type isoforms. Neuronal Ca2+ sensor-1 and CaBP5, both are calmodulin-like proteins, did not affect Na+, Ca2+ currents, and exocytosis. When expressed in cultured cortical neurons, the [Ca2+]
i
responses elicited by high-K+ depolarization were inhibited by CaBP1 isoforms. In HEK293T cells cotransfected with N-type Ca2+ channel and L-CaBP1, the current was reduced and activation curve was shifted positively. These results demonstrate the importance
of CaBP1s in modulating the stimulus-secretion coupling in excitable cells.
M.-L. Chen and Y.-C. Chen contributed equally to this study 相似文献
5.
Plant calcium pumps, similarly to animal Ca2+ pumps, belong to the superfamily of P-type ATPase comprising also the plasma membrane H+-ATPase of fungi and plants, Na+/K+ ATPase of animals and H+/K+ ATPase of mammalian gastric mucosa. According to their sensitivity to calmodulin the plant Ca2+-ATPases have been divided into two subgroups: type IIA (homologues of animal SERCA) and type IIB (homologues of animal PMCA).
Regardless of the similarities in a protein sequence, the plant Ca2+ pumps differ from those in animals in their cellular localization, structure and sensitivity to inhibitors. Genomic investigations
revealed multiplicity of plant Ca2+-ATPases; they are present not only in the plasma membranes and ER but also in membranes of most of the cell compartments,
such as vacuole, plastids, nucleus or Golgi apparatus. Studies using yeast mutants made possible the functional and biochemical
characterization of individual plant Ca2+-ATMPases. Plant calcium pumps play an essential role in signal transduction pathways, they are responsible for the regulation
of [Ca2+] in both cytoplasm and endomembrane compartments. These Ca2+-ATPases appear to be involved in plant adaptation to stress conditions, like salinity, chilling or anoxia. 相似文献
6.
Z. I. Krutetskaya L. S. Milenina A. A. Naumova S. N. Butov V. G. Antonov A. D. Nozdrachev 《Doklady. Biochemistry and biophysics》2017,472(1):74-76
Using Fura-2AM microfluorimetry, we have shown for the first time that sigma-1 receptor antagonist, antipsychotic haloperidol, significantly inhibits glutoxim- and molixan-induced Ca2+-response in peritoneal macrophages. These results indicate possible involvement of sigma-1 receptors in the signal cascade induced by glutoxim or molixan and leading to intracellular Ca2+ concentration increase in macrophages. 相似文献
7.
Mutoh H Yoshino M 《Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology》2004,174(1):21-28
The Ca2+-conducting pathway of myocytes isolated from the cricket lateral oviduct was investigated by means of the whole-cell patch clamp technique. In voltage-clamp configuration, two types of whole cell inward currents were identified. One was voltage-dependent, initially activated at –40 mV and reaching a maximum at 10 mV with the use of 140 mM Cs2+-aspartate in the patch pipette and normal saline in the bath solution. Replacement of the external Ca2+ with Ba2+ slowed the current decay. Increasing the external Ca2+ or Ba2+ concentration increased the amplitude of the inward current and the current–voltage (I–V) relationship was shifted as expected from a screening effect on negative surface charges. The inward current could be carried by Na+ in the absence of extracellular Ca2+. Current carried by Na+ (I
Na) was almost completely blocked by the dihydropyridine Ca2+ channel antagonist, nifedipine, suggesting that the I
Na is through voltage-dependent L-type Ca2+ channels. The other inward current is voltage-independent and its I–V relationship was linear between –100 mV to 0 mV with a slight inward rectification at more hyperpolarizing membrane potentials when 140 mM Cs+-aspartate and 140 mM Na+-gluconate were used in the patch pipette and in the bath solution, respectively. A similar current was observed even when the external Na+ was replaced with an equimolar amount of K+ or Cs+, or 50 mM Ca2+ or Ba2+. When the osmolarity of the bath solution was reduced by removing mannitol from the bath solution, the inward current became larger at negative potentials. The I–V relationship for the current evoked by the hypotonic solution also showed a linear relationship between –100 mV to 0 mV. Bath application of Gd3+ (10 M) decreased the inward current activated by membrane hyperpolarization. These results clearly indicate that the majority of current activated by a membrane hyperpolarization is through a stretch-activated Ca2+-permeable nonselective cation channel (NSCC). Here, for the first time, we have identified voltage-dependent L-type Ca2+ channel and stretch-activated Ca2+-permeable NSCCs from enzymatically isolated muscle cells of the cricket using the whole-cell patch clamp recording technique.Abbreviations
I
Ca
Ca2+ current
-
I
Na
Na+ current
-
I–V
current–voltage
-
NSCC
nonselective cation channel
Communicated by G. Heldmaier 相似文献
8.
Pia A. Elustondo Matthew Nichols George S. Robertson Evgeny V. Pavlov 《Journal of bioenergetics and biomembranes》2017,49(1):113-119
Calcium (Ca2+) plays diverse roles in all living organisms ranging from bacteria to humans. It is a structural element for bones, an essential mediator of excitation-contraction coupling, and a universal second messenger in the regulation of ion channel, enzyme and gene expression activities. In mitochondria, Ca2+ is crucial for the control of energy production and cellular responses to metabolic stress. Ca2+ uptake by the mitochondria occurs by the uniporter mechanism. The Mitochondrial Ca2+ Uniporter (MCU) protein has recently been identified as a core component responsible for mitochondrial Ca2+ uptake. MCU knockout (MCU KO) studies have identified a number of important roles played by this high capacity uptake pathway. Interestingly, this work has also shown that MCU-mediated Ca2+ uptake is not essential for vital cell functions such as muscle contraction, energy metabolism and neurotransmission. Although mitochondrial Ca2+ uptake was markedly reduced, MCU KO mitochondria still contained low but detectable levels of Ca2+. In view of the fundamental importance of Ca2+ for basic cell signalling, this finding suggests the existence of other currently unrecognized pathways for Ca2+ entry. We review the experimental evidence for the existence of alternative Ca2+ influx mechanisms and propose how these mechanisms may play an integral role in mitochondrial Ca2+ signalling. 相似文献
9.
In the present study, the effect of fluoride on intracellular free calcium ([Ca2+]i) and Ca2+-ATPase of renal cells were examined. Some paradoxical experimental results about the mechanism of fluoride toxicity were observed. In vivo, 48 Wistar rats were divided into 4 groups, and half of rats were treated with sodium fluoride (NaF) by drinking water (per liter of tap water containing 100 mg F-). Compared with the respective control, the level of [Ca2+]i of the kidney in two fluoride-treated rats obviously increased (p < 0.05); and the activity of Ca2+-ATPase in 100 mg F-/L groups with a standard diet did not significantly increase, and the enzyme activity in 100-mg F-/L group with a low-calcium diet decreased significantly compared to the 100 mg F-/L group with a standard diet (p < 0.05). In vitro, renal tubular cells were cultured and respectively exposed to 1.0, 5.0, 7.5, and 12.5 mg/L fluoride in the culture medium. Results showed the significantly elevated activity of Ca2+-ATPase in the cells exposed to 1.0 and 5.0 mg/L fluoride (p < 0.05), and this enzyme activity indicated inhibitory trend in cells of the 7.5- and 12.5-mg/L fluoride-treated group. To sum up, the effect of fluoride on Ca2+-ATPase is a similar to a dose-effect relationship phenomenon characterized by low-dose stimulation and high-dose inhibition, and the increase of [Ca2+]i probably plays a key role on the mechanism of renal injury in fluorosis. 相似文献
10.
Daniel C. Moreira-Lobo Jader S. Cruz Flavia R. Silva Fabíola M. Ribeiro Christopher Kushmerick Fernando A. Oliveira 《Cellular and molecular neurobiology》2017,37(3):453-460
Thiamine (vitamin B1) is co-factor for three pivotal enzymes for glycolytic metabolism: pyruvate dehydrogenase, α-ketoglutarate dehydrogenase, and transketolase. Thiamine deficiency leads to neurodegeneration of several brain regions, especially the cerebellum. In addition, several neurodegenerative diseases are associated with impairments of glycolytic metabolism, including Alzheimer’s disease. Therefore, understanding the link between dysfunction of the glycolytic pathway and neuronal death will be an important step to comprehend the mechanism and progression of neuronal degeneration as well as the development of new treatment for neurodegenerative states. Here, using an in vitro model to study the effects of thiamine deficiency on cerebellum granule neurons, we show an increase in Ca2+ current density and CaV1.2 expression. These results indicate a link between alterations in glycolytic metabolism and changes to Ca2+ dynamics, two factors that have been implicated in neurodegeneration. 相似文献
11.
Phosphorylation of the cardiac ryanodine receptor (RyR2) is thought to be important not only for normal cardiac excitation-contraction
coupling but also in exacerbating abnormalities in Ca2+ homeostasis in heart failure. Linking phosphorylation to specific changes in the single-channel function of RyR2 has proved
very difficult, yielding much controversy within the field. We therefore investigated the mechanistic changes that take place
at the single-channel level after phosphorylating RyR2 and, in particular, the idea that PKA-dependent phosphorylation increases
RyR2 sensitivity to cytosolic Ca2+. We show that hyperphosphorylation by exogenous PKA increases open probability (P
o) but, crucially, RyR2 becomes uncoupled from the influence of cytosolic Ca2+; lowering [Ca2+] to subactivating levels no longer closes the channels. Phosphatase (PP1) treatment reverses these gating changes, returning
the channels to a Ca2+-sensitive mode of gating. We additionally found that cytosolic incubation with Mg2+/ATP in the absence of exogenously added kinase could phosphorylate RyR2 in approximately 50% of channels, thereby indicating
that an endogenous kinase incorporates into the bilayer together with RyR2. Channels activated by the endogenous kinase exhibited
identical changes in gating behavior to those activated by exogenous PKA, including uncoupling from the influence of cytosolic
Ca2+. We show that the endogenous kinase is both Ca2+-dependent and sensitive to inhibitors of PKC. Moreover, the Ca2+-dependent, endogenous kinase–induced changes in RyR2 gating do not appear to be related to phosphorylation of serine-2809.
Further work is required to investigate the identity and physiological role of this Ca2+-dependent endogenous kinase that can uncouple RyR2 gating from direct cytosolic Ca2+ regulation. 相似文献
12.
Jiayu Liu Yufan Niu Jingjing Zhang Yuqing Zhou Zheng Ma Xuan Huang 《Plant Cell, Tissue and Organ Culture》2018,132(3):413-424
Calcium (Ca2+) signals are essential transducers and regulators in many adaptive and developmental processes in plants. Protective responses of plants to a variety of environmental stress factors are mediated by transient changes of Ca2+ concentration in plant cells. Ca2+ ions are quickly transported by channel proteins present on the plasma membrane. During responses to external stimuli, various signal molecules are transported directly from extracellular to intracellular compartments via Ca2+ channel proteins. Three types of Ca2+ channels have been identified in plant cell membranes: voltage-dependent Ca2+-permeable channels (VDCCs), which is sorted to depolarization-activated Ca2+-permeable channels (DACCs) and hyperpolarization-activated Ca2+-permeable channels (HACCs), voltage-independent Ca2+-permeable channels (VICCs). They make functions in the abiotic stress such as TPCs, CNGCs, MS channels, annexins which distribute in the organelles, plasma membrane, mitochondria, cytosol, intracelluar membrane. This review summarizes recent advances in our knowledge of many types of Ca2+ channels and Ca2+ signals involved in abiotic stress resistance and responses in plant cells. 相似文献
13.
A kinetic model for the membrane Ca2+-ATPase is considered. The catalytic cycle in the model is extended by enzyme auto-inhibition and by oscillatory calcium influx. It is shown that the conductive enzyme activity can be registered as damped or sustained Ca2+ pulses similar to observed experimentally. It is shown that frequency variations in Ca2+ oscillatory influx induce changes of pulsating enzyme activity. Encoding is observed for the signal frequency into a number of fixed levels of sustained pulses in the enzyme activity. At certain calcium signal frequencies, the calculated Ca2+-ATPase conductivity demonstrates chaotic multi-level pulses, similar to those observed experimentally.__________Translated from Biokhimiya, Vol. 70, No. 4, 2005, pp. 539–544.Original Russian Text Copyright © 2005 by Goldstein, Mayevsky, Zakrjevskaya. 相似文献
14.
15.
The anoxia-dependent elevation of cytosolic Ca2+ concentration, [Ca2+]cyt, was investigated in plants differing in tolerance to hypoxia. The [Ca2+]cyt was measured by fluorescence microscopy in single protoplasts loaded with the calcium-fluoroprobe Fura 2-AM. Imposition of
anoxia led to a fast (within 3 min) significant elevation of [Ca2+]cyt in rice leaf protoplasts. A tenfold drop in the external Ca2+ concentration (to 0.1 mM) resulted in considerable decrease of the [Ca2+]cyt shift. Rice root protoplasts reacted upon anoxia with higher amplitude. Addition of plasma membrane (verapamil, La3+ and EGTA) and intracellular membrane Ca2+-channel antagonists (Li+, ruthenium red and cyclosporine A) reduced the anoxic Ca2+-accumulation in rice. Wheat protoplasts responded to anoxia by smaller changes of [Ca2+]cyt. In wheat leaf protoplasts, the amplitude of the Ca2+-shift little depended on the external level of Ca2+. Wheat root protoplasts were characterized by a small shift of [Ca2+]cyt under anoxia. Plasmalemma Ca2+-channel blockers had little effect on the elevation of cytosolic Ca2+ in wheat protoplasts. Intact rice seedlings absorbed Ca2+ from the external medium under anoxic treatment. On the contrary, wheat seedlings were characterized by leakage of Ca2+. Verapamil abolished the Ca2+ influx in rice roots and Ca2+ efflux from wheat roots. Anoxia-induced [Ca2+]cyt elevation was high particularly in rice, a hypoxia-tolerant species. In conclusion, both external and internal Ca2+ stores are important for anoxic [Ca2+]cyt elevation in rice, whereas the hypoxia-intolerant wheat does not require external sources for [Ca2+]cyt rise. Leaf and root protoplasts similarly responded to anoxia, independent of their organ origin. 相似文献
16.
I. V. Shemarova V. P. Nesterov 《Journal of Evolutionary Biochemistry and Physiology》2008,44(4):399-413
The review considers mechanisms of Ca2+-dependent regulation of cell growth, differentiation, and apoptosis in cells of the higher eukaryotes by modulation of the signal Ras-MAPK pathway. 相似文献
17.
The basic mechanisms of regulation of Ca2+ influx have been studied in murine myoblasts proliferating and differentiating in culture. The presence of L-type Ca2+ channels in proliferating myoblasts is shown for the first time. It is also shown that the influx of Ca2+ through these channels is regulated by the adrenergic system. The influx of Ca2+ after activation of the adrenergic system by addition of adrenaline has been estimated in comparison with the contribution
of reticular stocks exhausted by ATP in calcium-free medium. The Ca2+ influx in proliferating myoblasts is regulated by β-2 adrenergic receptors whose action is mediated by adenylate cyclase
through L-type calcium channels. In differentiating myoblasts, the adrenaline-induced Ca2+ influx is substantially lower than in proliferating cells, and maximal influx of Ca2+ may be reached only upon exhaustion of reticular stocks. 相似文献
18.
Nicotinic acid dinucleotide phosphate (NAADP) is unique amongst Ca2+ mobilizing messengers in that its principal function is to mobilize Ca2+ from acidic organelles. Early studies indicated that it was likely that NAADP activates a novel Ca2+ release channel distinct from the well characterized Ca2+ release channels on the (sarco)-endoplasmic reticulum (ER), inositol trisphosphate and ryanodine receptors. In this review,
we discuss the emergence of a novel family of endolysosomal channels, the two-pore channels (TPCs), as likely targets for
NAADP, and how molecular and pharmacological manipulation of these channels is enhancing our understanding of the physiological
roles of NAADP as an intracellular Ca2+ mobilizing messenger. 相似文献
19.
In the absence of exogenous Ca2+ and Mg2+ and in the presence of EGTA, which favours the release of endogenous Ca2+, the polyamine spermine is able to stimulate the activity of pyruvate dehydrogenase complex (PDC) of energized rat liver
mitochondria (RLM). This stimulation exhibits a gradual concentration-dependent trend, which is maximum, about 140%, at 0.5 mM
concentration, after 30 min of incubation. At concentrations higher than 0.5 mM, spermine still stimulates PDC, when compared
with the control, but shows a slight dose-dependent decrease. Changes in PDC stimulation are very close to the phosphorylation
level of the E1α subunit of PDC, which regulates the activity of the complex, but it is also the target of spermine. In other words, progressive
dephosphorylation gradually enhances the stimulation of RLM and progressive phosphorylation slightly decreases it. These results
provide the first evidence that, when transported in RLM, spermine can interact in various ways with PDC, showing dose-dependent
behaviour. The interaction most probably takes place directly on a specific site for spermine on one of the regulatory enzymes
of PDC, i.e. pyruvate dehydrogenase phosphatase (PDP). The interaction of spermine with PDC may also involve activation of
another regulatory enzyme, pyruvate dehydrogenase kinase (PDK), resulting in an increase in E1α phosphorylation and consequently reduced stimulation of PDC at high polyamine concentrations. The different effects of spermine
in RLM are discussed, considering the different activities of PDP and PDK isoenzymes. It is suggested that the polyamine at
low concentrations stimulates the isoenzyme PDP2 and at high concentrations it stimulates PDK2. 相似文献
20.
The human formyl peptide receptor like 1 (FPRL-1) is a variant of the Gi-coupled formyl-peptide receptor. Functional FPRL-1 is endogenously expressed in the U87 astrocytoma cell line and there is
accumulating evidence to suggest that FPRL-1 may be involved in neuroinflammation associated with the pathogenesis of Alzheimer’s
disease. In this study, we examined the ability of FPRL-1 to mobilize intracellular Ca2+ in U87 astrocytoma cells, as well as in Chinese hamster ovary (CHO) cells stably expressing FPRL-1. We showed that Trp–Lys–Tyr–Met–Val–Met–NH2 (WKYMVM), a specific agonist for FPRL-1, stimulated Ca2+ influx in both U87 and FPRL-1/CHO cells. These effects can be inhibited by the FPRL-1 selective antagonist, WRW4. Involvement of Gi proteins was demonstrated with the use of pertussis toxin, while inhibitors of store-operated channels (SOC) including 1-[2-(4-methoxyphenyl)]-2-[3-(4-methpxyphenyl)propoxy]ethyl-1H-imidazole hydrochloride (SKF96365) and 2-aminoethoxydiphenyl borate (2-APB) were found to abolish the WKYMVM-induced Ca2+ increase. However, intracellular Ca2+ mobilization in both cell lines were unaffected by the phospholipase Cβ inhibitor U73122 or selective ryanodine receptor
inhibitors. Our data demonstrated that activation of Gi-coupled FPRL-1 can lead to Ca2+ influx possibly via SOCs in U87 and FPRL-1/CHO cells. 相似文献