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1.
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
2.
Intracellular Ca2+ is vital for cell physiology. Disruption of Ca2+ homeostasis contributes to human diseases such as heart failure, neuron-degeneration, and diabetes. To ensure an effective
intracellular Ca2+ dynamics, various Ca2+ transport proteins localized in different cellular regions have to work in coordination. The central role of mitochondrial
Ca2+ transport mechanisms in responding to physiological Ca2+ pulses in cytosol is to take up Ca2+ for regulating energy production and shaping the amplitude and duration of Ca2+ transients in various micro-domains. Since the discovery that isolated mitochondria can take up large quantities of Ca2+ approximately 5 decades ago, extensive studies have been focused on the functional characterization and implication of ion
channels that dictate Ca2+ transport across the inner mitochondrial membrane. The mitochondrial Ca2+ uptake sensitive to non-specific inhibitors ruthenium red and Ru360 has long been considered as the activity of mitochondrial
Ca2+ uniporter (MCU). The general consensus is that MCU is dominantly or exclusively responsible for the mitochondrial Ca2+ influx. Since multiple Ca2+ influx mechanisms (e.g. L-, T-, and N-type Ca2+ channel) have their unique functions in the plasma membrane, it is plausible that mitochondrial inner membrane has more than
just MCU to decode complex intracellular Ca2+ signaling in various cell types. During the last decade, four molecular identities related to mitochondrial Ca2+ influx mechanisms have been identified. These are mitochondrial ryanodine receptor, mitochondrial uncoupling proteins, LETM1
(Ca2+/H+ exchanger), and MCU and its Ca2+ sensing regulatory subunit MICU1. Here, we briefly review recent progress in these and other reported mitochondrial Ca2+ influx pathways and their differences in kinetics, Ca2+ dependence, and pharmacological characteristics. Their potential physiological and pathological implications are also discussed. 相似文献
3.
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
4.
P. M. Abdul-Muneer Mathew Long Adriano Andrea Conte Vijayalakshmi Santhakumar Bryan J. Pfister 《Molecular neurobiology》2017,54(6):3964-3975
We investigated the hypothesis that high Ca2+ influx during traumatic brain injury induces the activation of the caspase-1 enzyme, which triggers neuroinflammation and cell apoptosis in a cell culture model of neuronal stretch injury and an in vivo model of fluid percussion injury (FPI). We first established that stretch injury causes a rapid increase in the intracellular Ca2+ level, which activates interleukin-converting enzyme caspase-1. The increase in the intracellular Ca2+ level and subsequent caspase-1 activation culminates into neuroinflammation via the maturation of IL-1β. Further, we analyzed caspase-1-mediated apoptosis by TUNEL staining and PARP western blotting. The voltage-gated sodium channel blocker, tetrodotoxin, mitigated the stretch injury-induced neuroinflammation and subsequent apoptosis by blocking Ca2+ influx during the injury. The effect of tetrodotoxin was similar to the caspase-1 inhibitor, zYVAD-fmk, in neuronal culture. To validate the in vitro results, we demonstrated an increase in caspase-1 activity, neuroinflammation and neurodegeneration in fluid percussion-injured animals. Our data suggest that neuronal injury/traumatic brain injury (TBI) can induce a high influx of Ca2+ to the cells that cause neuroinflammation and cell death by activating caspase-1, IL-1β, and intrinsic apoptotic pathways. We conclude that excess IL-1β production and cell death may contribute to neuronal dysfunction and cognitive impairment associated with TBI. 相似文献
5.
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
6.
Summary In this study, the toxic effect of sanguinarine (SANG) on heart was studied with isolated cardiac muscle strip isolated from Wistar rat. SANG induced positive inotropic action followed by contracture on the left ventricle and both atria strips. In addition, SANG dose-dependently inhibited spontaneous beat of the right atrium. SANG-induced contracture was completely suppressed by pretreatment with La3+ or in a Ca2+ free Tyrode solution containing 2.5 mM EGTA. Incubating isolated cardiomyocytes with SANG enhanced the 45Ca2+ influx, which could be inhibited by pretreatment with La3+. However, the SANG-induced 45Ca2+ influx could not be inhibited by pretreatment with other Ca2+ channel blockers, such as nifedipine, verapamil, diltiazem, nickel and manganese, and amiloride. Although antioxidants can inhibit the SANG-induced lipid peroxidation, they could not prevent the SANG-induced contracture. N-acetylcysteine and dithiothreitol, the sulfhydryl reducing agents, were shown to be effective in preventing the SANG-induced contracture. These data suggested that the SANG-induced contracture is caused by the influx of extracellular Ca2+ through a La3+-sensitive Ca2+ channel. 相似文献
7.
The American alligator can hibernate during winter, which may lead to osmotic imbalance because of reduced kidney function
and lack of food consumption during this period. Accordingly, we hypothesized that their red blood cells would have a well-developed
regulatory volume decrease (RVD) to cope with the homeostatic challenges associated with torpor. Osmotic fragility was determined
optically, mean cell volume was measured by electronic sizing, and changes in intracellular Ca2+ concentration were visualized using fluorescence microscopy and fluo-4-AM. Osmotic fragility increased and the ability to
regulate volume was inhibited when extracellular Na+ was replaced with K+, or when cells were exposed to the K+ channel inhibitor quinine, indicating a requirement of K+ efflux for RVD. Addition of the ionophore gramicidin to the extracellular medium decreased osmotic fragility and also potentiated
volume recovery, even in the presence of quinine. In addition, hypotonic shock (0.5× Ringer) caused an increase in cytosolic
Ca2+, which resulted from Ca2+ influx because it was not observed when extracellular Ca2+ was chelated with EGTA (ethylene glycol-bis(2-aminoethylether)-N,N,N′,N′-tetraacetic acid). Furthermore, cells loaded with BAPTA-AM (1,2-bis(2-aminophenoxymethyl)ethane-N,N,N′,N′-tetraacetic acid tetrakis(acetoxymethyl) ester) or exposed to a low Ca2+-EGTA hypotonic Ringer had a greater osmotic fragility and also failed to recover from cell swelling, indicating that extracellular
Ca2+ was needed for RVD. Gramicidin reversed the inhibitory effect of low extracellular Ca2+. Finally, and surprisingly, the Ca2+ ionophore A23187 increased osmotic fragility and inhibited volume recovery. Taken together, our results show that cell swelling
activated a K+ permeable pathway via a Ca2+-dependent mechanism, and this process mediated K+ loss during RVD. 相似文献
8.
The objective of this study was to investigate the influences of carbonyl stress induced by malondialdehyde (MDA), a typical
intermediate of lipid peroxidation, on intracellular free Ca2+ concentration ([Ca2+]i) alterations in cultured hippocampal neurons of rat. The microphotographic study clearly demonstrated that the hippocampal
neurons became gradually damaged following exposure to different concentrations of MDA. Further study indicated that the plasma
membrane Ca2+-ATPase (PMCA) activity was inhibited by MDA in a concentration- and time-dependent manner. The supplementation of 100 μM
MDA was found to cause a notable early phase increase of [Ca2+]i in hippocampal neuron cultures followed by a more pronounced late-phase elevation of [Ca2+]i. Such effect of MDA was prevented by the addition of nimodipine, an inhibitor of L-type calcium channel or by an extracellular
Ca2+ chelator EGTA. The identification of the calcium signalling pathways were studied by applying U73122, an inhibitor of PL-C,
and H-89, an inhibitor of protein kinase A (PKA), showing the involvement of PL-C/IP3 pathway but not the PKA/cAMP pathway.
These results suggested that MDA-related carbonyl stress caused damages of rat hippocampal neurons by triggering Ca2+ influx and influencing Ca2+ homeostasis in cultured neurons, and also MDA may act as a signalling molecule regulating Ca2+ release from intracellular stores. 相似文献
9.
10.
Capo JA Mandal PK Eyyunni S Ahearn GA 《Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology》2005,175(1):13-20
The lobster (Homarus americanus) hepato-pancreatic epithelial baso-lateral cell membrane possesses three transport proteins that transfer calcium between the cytoplasm and hemolymph: an ATP-dependent calcium ATPase, a sodium-calcium exchanger, and a verapamil-sensitive cation channel. We used standard centrifugation methods to prepare purified hepato-pancreatic baso-lateral membrane vesicles and a rapid filtration procedure to investigate whether 65Zn2+ transfer across this epithelial cell border occurs by any of these previously described transporters for calcium. Baso-lateral membrane vesicles were osmotically reactive and exhibited a time course of uptake that was linear for 10–15 s and approached equilibrium by 120 s. In the absence of sodium, 65Zn2+ influx was a hyperbolic function of external zinc concentration and followed the Michaelis-Menten equation for carrier transport. This carrier transport was stimulated by the addition of 150 M ATP (increase in Km and Jmax) and inhibited by the simultaneous presence of 150 mol l–1 ATP+250 mol l–1 vanadate (decrease in both Km and Jmax). In the absence of ATP, 65Zn2+ influx was a sigmoidal function of preloaded vesicular sodium concentration (0, 5, 10, 20, 30, 45, and 75 mmol l–1) and exhibited a Hill Coefficient of 4.03±1.14, consistent with the exchange of 3 Na+/1Zn2+. Using Dixon analysis, calcium was shown to be a competitive inhibitor of baso-lateral membrane vesicle 65Zn2+ influx by both the ATP-dependent (Ki=205 nmol l–1 Ca2+) and sodium-dependent (Ki=2.47 mol l–1 Ca2+) transport processes. These results suggest that zinc transport across the lobster hepato-pancreatic baso-lateral membrane largely occurred by the ATP-dependent calcium ATPase and sodium-calcium exchanger carrier proteins.Communicated by: I.D. Hume 相似文献
11.
Xiang Zhao Xiao-wei Zhao Hui He Yan-xiao Wang Xiao Zhang 《Journal of Plant Biology》2010,53(4):275-281
Our previous studies suggested the cross talk of nitric oxide (NO) with Ca2+ in regulating stomatal movement. However, its mechanism of action is not well defined in plant roots. In this study, sodium
nitroprusside (SNP, a NO donor) showed an inhibitory effect on the growth of wheat seedling roots in a dose-dependent manner,
which was alleviated through reducing extracellular Ca2+ concentration. Analyzing the content of Ca2+ and K+ in wheat seedling roots showed that SNP significantly promoted Ca2+ accumulation and inhibited K+ accumulation at a higher concentration of extracellular Ca2+, but SNP promoted K+ accumulation in the absence of extracellular Ca2+. To gain further insights into Ca2+ function in the NO-regulated growth of wheat seedling roots, we conducted the patch-clamped protoplasts of wheat seedling
roots in a whole cell configuration. In the absence of extracellular Ca2+, NO activated inward-rectifying K+ channels, but had little effects on outward-rectifying K+ channels. In the presence of 2 mmol L−1 CaCl2 in the bath solution, NO significantly activated outward-rectifying K+ channels, which was partially alleviated by LaCl3 (a Ca2+ channel inhibitor). In contrast, 2 mmol L−1 CaCl2 alone had little effect on inward or outward-rectifying K+ channels. Thus, NO inhibits the growth of wheat seedling roots likely by promoting extracellular Ca2+ influx excessively. The increase in cytosolic Ca2+ appears to inhibit K+ influx, promotes K+ outflux across the plasma membrane, and finally reduces the content of K+ in root cells. 相似文献
12.
Powered by the mitochondrial membrane potential, Ca2+ permeates the mitochondria via a Ca2+ channel termed Ca2+ uniporter and is pumped out by a Na+/Ca2+ exchanger, both of which are located on the inner mitochondrial membrane. Mitochondrial Ca2+ transients are critical for metabolic activity and regulating global Ca2+ responses. On the other hand, failure to control mitochondrial Ca2+ is a hallmark of ischemic and neurodegenerative diseases. Despite their importance, identifying the uniporter and exchanger remains elusive and their inhibitors are non-specific. This review will focus on the mitochondrial exchanger, initially describing how it was molecularly identified and linked to a novel member of the Na+/Ca2+ exchanger superfamily termed NCLX. Molecular control of NCLX expression provides a selective tool to determine its physiological role in a variety of cell types. In lymphocytes, NCLX is essential for refilling the endoplasmic reticulum Ca2+ stores required for antigendependent signaling. Communication of NCLX with the store-operated channel in astroglia controls Ca2+ influx and thereby neuro-transmitter release and cell proliferation. The refilling of the Ca2+ stores in the sarcoplasmic reticulum, which is controlled by NCLX, determines the frequency of action potential and Ca2+ transients in cardiomyocytes. NCLX is emerging as a hub for integrating glucose-dependent Na+ and Ca2+ signaling in pancreatic β cells, and the specific molecular control of NCLX expression resolved the controversy regarding its role in neurons and β cells. Future studies on an NCLX knockdown mouse model and identification of human NCLX mutations are expected to determine the role of mitochondrial Ca2+ efflux in organ activity and whether NCLX inactivation is linked to ischemic and/or neurodegenerative syndromes. Structure-function analysis and protein analysis will identify the NCLX mode of regulation and its partners in the inner membrane of the mitochondria. 相似文献
13.
Xu-Dong Feng Qing Xia Lan Yuan Hai-Feng Huang Xiao-Da Yang Kui Wang 《Cell biology and toxicology》2011,27(1):1-12
Gadolinium (Gd) and its complexes are utilized widely in industrial and clinical diagnoses. As a rare earth metal ion, free
gadolinium (Gd3+) in the human body poses neurotoxic risks during its in vivo release and retention. In the central nervous system, astrocytes
play a pivotal role in processing toxic metal ions. The present study evaluates the effects of Gd on cellular calcium homeostasis,
a common mechanism that causes cell death, and on unfolded protein responses (UPRs), a mechanism for cell survival in response
to toxic stimuli in mammalian cells. The experimental results indicate that the influx of extracellular Ca2+ increases greatly after the exposure of astrocytes to Gd; however, no cell deaths were observed. Further evidence suggests
the up-regulated expression of the endoplasmic reticulum (ER)-resident chaperone protein GRP78 by ER stress-mediated signal
transductions, specifically the activation of ATF6, eIF2a, and IRE1. These results suggest that Gd promotes Ca2+ influx, thus triggering UPRs, which can be closely associated to the resistance of astrocytes to Gd-induced cytotoxicity. 相似文献
14.
The plasma membrane calcium ATPases (PMCA) are a family of genes which extrude Ca2+ from the cell and are involved in the maintenance of intracellular free calcium levels and/or with Ca2+ signalling, depending on the cell type. In the cardiovascular system, Ca2+ is not only essential for contraction and relaxation but also has a vital role as a second messenger in signal transduction
pathways. A complex array of mechanisms regulate intracellular free calcium levels in the heart and vasculature and a failure
in these systems to maintain normal Ca2+ homeostasis has been linked to both heart failure and hypertension. This article focuses on the functions of PMCA, in particular
isoform 4 (PMCA4), in the heart and vasculature and the reported links between PMCAs and contractile function, cardiac hypertrophy,
cardiac rhythm and sudden cardiac death, and blood pressure control and hypertension. It is becoming clear that this family
of calcium extrusion pumps have essential roles in both cardiovascular health and disease. 相似文献
15.
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
16.
In an earlier study, we showed that mitochondria hyperpolarized after short periods of oxygen-glucose deprivation (OGD), and
this response appeared to be associated with subsequent apoptosis or survival. Here, we demonstrated that hyperpolarization
following short periods of OGD (30 min; 30OGD group) increased the cytosolic Ca2+ ([Ca2+]c) buffering capacity in mitochondria. After graded OGD (0 min (control), 30 min, 120 min), rat cultured hippocampal neurons
were exposed to glutamate, evoking Ca2+influx. The [Ca2+]c level increased sharply, followed by a rapid increase in mitochondrial Ca2+ [Ca2+]m. The increase in the [Ca2+]m level accompanied a reduction in the [Ca2+]c level. After reaching a peak, the [Ca2+]c level decreased more rapidly in the 30OGD group than in the control group. This buffering reaction was pronounced in the
30OGD group, but not in the 120OGD group. The enhanced buffering capacity of the mitochondria may be linked to preconditioning
after short-term ischemic episodes. 相似文献
17.
W. M. MacKenzie S. F. Perry 《Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology》1997,167(1):52-60
Whole body calcium influx, branchial calcium efflux, and renal Ca2+ excretion were measured in rainbow trout (Oncorhynchus mykiss) exposed to hypercapnia. These experiments were performed to assess the potential impact on Ca2+ balance of the changes in gill morphology known to accompany respiratory acidosis in this species. After 48 h of hypercapnia,
gill filamental chloride cell fractional area was significantly reduced. Despite this reduction and the presumed involvement
of the chloride cell in calcium influx, whole body calcium influx was increased after 12 h of hypercapnia and remained elevated
for 48 h. Branchial calcium efflux was unaltered during hypercapnia exposure, whereas renal Ca2+ excretion was elevated over preflux values only at 6 h of hypercapnia. Measurement of the kinetics of whole body calcium
influx after 48 h of hypercapnia revealed a significant increase in the maximal uptake rate of Ca2+, yet the affinity constant of Ca2+ uptake was unaffected. Measurements of high-affinity Ca2+ -ATPase activities and ATP-dependent Ca2+ transport of gill basolateral membrane vesicles revealed that the ATP-dependent Ca2+ extrusion mechanism of the gills was not affected by hypercapnia. The results of the present study clearly show that the
reduced chloride cell surface area that accompanies hypercapnia in trout does not impair calcium homeostasis. Although adjustments
to the basolateral membrane high affinity Ca2+ transporter do not appear to play a role, the mechanism(s) underlying the maintenance of calcium homeostasis under hypercapnic
conditions are unresolved.
Accepted: 1 July 1996 相似文献
18.
Patrícia Nardin Lucas Tortorelli André Quincozes-Santos Lúcia Maria V. de Almeida Marina C. Leite Ana Paula Thomazi Carmem Gottfried Susana T. Wofchuk Rosario Donato Carlos-Alberto Gonçalves 《Neurochemical research》2009,34(9):1603-1611
Hippocampal slices have been widely used to investigate electrophysiological and metabolic neuronal parameters, as well as
parameters of astroglial activity including protein phosphorylation and glutamate uptake. S100B is an astroglial-derived protein,
which extracellularly plays a neurotrophic activity during development and excitotoxic insult. Herein, we characterized S100B
secretion in acute hippocampal slices exposed to different concentrations of K+ and Ca2+ in the extracellular medium. Absence of Ca2+ and/or low K+ (0.2 mM KCl) caused an increase in S100B secretion, possibly by mobilization of internal stores of Ca2+. In contrast, high K+ (30 mM KCl) or calcium channel blockers caused a decrease in S100B secretion. This study suggests that exposure of acute
hippocampal slices to low- and high-K+ could be used as an assay to evaluate astrocyte activity by S100B secretion: positively regulated by low K+ (possibly involving mobilization of internal stores of Ca2+) and negatively regulated by high-K+ (likely secondary to influx of K+). 相似文献
19.
Mears D 《The Journal of membrane biology》2004,200(2):57-66
Insulin secretion from β-cells of the pancreatic islets of Langerhans is triggered by Ca2+ influx through voltage-dependent Ca2+ channels. Electrophysiological and molecular studies indicate that β-cells express several subtypes of these channels. This review discusses their roles in regulating insulin secretion, focusing on recent studies using β-cells, exogenous expression systems, and Ca2+ channel knockout mice. These investigations reveal that L-type Ca2+ channels in the β-cell physically interact with the secretory apparatus by binding to synaptic proteins on the plasma membrane and insulin granule. As a result, Ca2+ influx through L-type channels efficiently and rapidly stimulates release of a pool of insulin granules in close contact with the channels. Thus, L-type Ca2+ channel activity is preferentially coupled to exocytosis in the β-cell, and plays a critical role in regulating the dynamics of insulin secretion. Non-L-type channels carry a significant portion of the total voltage-dependent Ca2+ current in β-cells and cell lines from some species, but nevertheless account for only a small fraction of insulin secretion. These channels may regulate exocytosis indirectly by affecting membrane potential or second messenger signaling pathways. Finally, voltage-independent Ca2+ entry pathways and their potential roles in β-cell function are discussed. The emerging picture is that Ca2+ channels regulate insulin secretion at multiple sites in the stimulus-secretion coupling pathway, with the specific role of each channel determined by its biophysical and structural properties.This revised version was published online in June 2005 with a corrected cover date. 相似文献
20.
O. V. Kozlova S. Yu. Egorov F. G. Kupriyanova-Ashina Nick Rid G. I. El’-Registan 《Microbiology》2004,73(6):629-634
Using the mutant strain Aspergillus awamori 66A, producing the recombinant Ca2+-dependent photosensitive protein aequorin, the dynamics of Ca2+ was studied for the first time in the cytosol of micromycetes exposed to stressful factors, such as an increase in extracellular Ca2+ to 50 mM, hypoosmotic shock, and mechanical shock. The cell response to stress proved to involve an increase in the Ca2+ concentration in the cytosol, which was determined from the amplitude of aequorin luminescence and the time of the amplitude enhancement and relaxation. The level of the Ca2+ response depended on the physiological stimulus. Inhibitory analysis with various agents that block Ca2+ channels and with agonists that specifically enhance the activity of the channels suggested that (1) the level of Ca2+ in the cytosol of micromycetes increases in response to stress because of the ion influx from both the growth medium and intracellular reservoirs and (2) potential-dependent transport systems play the major role in the Ca2+ influx into the cytosol of the micromycete cells.Translated from Mikrobiologiya, Vol. 73, No. 6, 2004, pp. 734–740.Original Russian Text Copyright © 2004 by Kozlova, Egorov, Kupriyanova-Ashina, Rid, El-Registan. 相似文献