共查询到20条相似文献,搜索用时 28 毫秒
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Eitaro Aihara Courtney L. Hentz Abraham M. Korman Nicholas P. J. Perry Vikram Prasad Gary E. Shull Marshall H. Montrose 《The Journal of biological chemistry》2013,288(47):33585-33597
We report that a localized intracellular and extracellular Ca2+ mobilization occurs at the site of microscopic epithelial damage in vivo and is required to mediate tissue repair. Intravital confocal/two-photon microscopy continuously imaged the surgically exposed stomach mucosa of anesthetized mice while photodamage of gastric epithelial surface cells created a microscopic lesion that healed within 15 min. Transgenic mice with an intracellular Ca2+-sensitive protein (yellow cameleon 3.0) report that intracellular Ca2+ selectively increases in restituting gastric epithelial cells adjacent to the damaged cells. Pretreatment with U-73122, indomethacin, 2-aminoethoxydiphenylborane, or verapamil inhibits repair of the damage and also inhibits the intracellular Ca2+ increase. Confocal imaging of Fura-Red dye in luminal superfusate shows a localized extracellular Ca2+ increase at the gastric surface adjacent to the damage that temporally follows intracellular Ca2+ mobilization. Indomethacin and verapamil also inhibit the luminal Ca2+ increase. Intracellular Ca2+ chelation (1,2-bis(o-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid/acetoxymethyl ester, BAPTA/AM) fully inhibits intracellular and luminal Ca2+ increases, whereas luminal calcium chelation (N-(2-hydroxyetheyl)-ethylendiamin-N,N,N′-triacetic acid trisodium, HEDTA) blocks the increase of luminal Ca2+ and unevenly inhibits late-phase intracellular Ca2+ mobilization. Both modes of Ca2+ chelation slow gastric repair. In plasma membrane Ca-ATPase 1+/− mice, but not plasma membrane Ca-ATPase 4−/− mice, there is slowed epithelial repair and a diminished gastric surface Ca2+ increase. We conclude that endogenous Ca2+, mobilized by signaling pathways and transmembrane Ca2+ transport, causes increased Ca2+ levels at the epithelial damage site that are essential to gastric epithelial cell restitution in vivo. 相似文献
3.
TRPM2 is a Ca2+-permeable non-selective cation channel that can be activated by adenosine dinucleotides, hydrogen peroxide, or intracellular Ca2+. The protein is expressed in a wide variety of cells, including neurons in the brain, immune cells, endocrine cells, and endothelial cells. This channel is also well expressed in β-cells in the pancreas. Insulin secretion from pancreatic β-cells is the primary mechanism by which the concentration of blood glucose is reduced. Thus, impairment of insulin secretion leads to hyperglycemia and eventually causes diabetes. Glucose is the principal stimulator of insulin secretion. The primary pathway involved in glucose-stimulated insulin secretion is the ATP-sensitive K+ (KATP) channel to voltage-gated Ca2+ channel (VGCC)-mediated pathway. Increases in the intracellular Ca2+ concentration are necessary for insulin secretion, but VGCC is not sufficient to explain [Ca2+]i increases in pancreatic β-cells and the resultant secretion of insulin. In this review, we focus on TRPM2 as a candidate for a [Ca2+]i modulator in pancreatic β-cells and its involvement in insulin secretion and development of diabetes. Although further analyses are needed to clarify the mechanism underlying TRPM2-mediated insulin secretion, TRPM2 could be a key player in the regulation of insulin secretion and could represent a new target for diabetes therapy. 相似文献
4.
The rise in intracellular Ca2+ mediated by AMPA subtype of glutamate receptors has been implicated in the pathogenesis of motor neuron disease, but the exact route of Ca2+ entry into motor neurons is not clearly known. In the present study, we examined the role of voltage gated calcium channels (VGCCs) in AMPA induced Ca2+ influx and subsequent intracellular signaling events responsible for motor neuron degeneration. AMPA stimulation caused sodium influx in spinal neurons that would depolarize the plasma membrane. The AMPA induced [Ca2+]i rise in motor neurons as well as other spinal neurons was drastically reduced when extracellular sodium was replaced with NMDG, suggesting the involvement of voltage gated calcium channels. AMPA mediated rise in [Ca2+]i was significantly inhibited by L-type VGCC blocker nifedipine, whereas ω-agatoxin-IVA and ω-conotoxin-GVIA, specific blockers of P/Q type and N-type VGCC were not effective. 1-Napthyl-acetyl spermine (NAS), an antagonist of Ca2+ permeable AMPA receptors partially inhibited the AMPA induced [Ca2+]i rise but selectively in motor neurons. Measurement of AMPA induced currents in whole cell voltage clamp mode suggests that a moderate amount of Ca2+ influx occurs through Ca2+ permeable AMPA receptors in a subpopulation of motor neurons. The AMPA induced mitochondrial calcium loading [Ca2+]m, mitochondrial depolarization and neurotoxicity were also significantly reduced in presence of nifedipine. Activation of VGCCs by depolarizing concentration of KCl (30 mM) in extracellular medium increased the [Ca2+]i but no change was observed in mitochondrial Ca2+ and membrane potential. Our results demonstrate that a subpopulation of motor neurons express Ca2+ permeable AMPA receptors, however the larger part of Ca2+ influx occurs through L-type VGCCs subsequent to AMPA receptor activation and consequent mitochondrial dysfunction is the trigger for motor neuron degeneration. Nifedipine is an effective protective agent against AMPA induced mitochondrial stress and degeneration of motor neurons. 相似文献
5.
Dissecting out the Complex Ca2+-Mediated Phenylephrine-Induced Contractions of Mouse Aortic Segments
Paul Fransen Cor E. Van Hove Arthur J. A. Leloup Wim Martinet Guido R. Y. De Meyer Katrien Lemmens Hidde Bult Dorien M. Schrijvers 《PloS one》2015,10(3)
L-type Ca2+ channel (VGCC) mediated Ca2+ influx in vascular smooth muscle cells (VSMC) contributes to the functional properties of large arteries in arterial stiffening and central blood pressure regulation. How this influx relates to steady-state contractions elicited by α1-adrenoreceptor stimulation and how it is modulated by small variations in resting membrane potential (Vm) of VSMC is not clear yet. Here, we show that α1-adrenoreceptor stimulation of aortic segments of C57Bl6 mice with phenylephrine (PE) causes phasic and tonic contractions. By studying the relationship between Ca2+ mobilisation and isometric tension, it was found that the phasic contraction was due to intracellular Ca2+ release and the tonic contraction determined by Ca2+ influx. The latter component involves both Ca2+ influx via VGCC and via non-selective cation channels (NSCC). Influx via VGCC occurs only within the window voltage range of the channel. Modulation of this window Ca2+ influx by small variations of the VSMC Vm causes substantial effects on the contractile performance of aortic segments. The relative contribution of VGCC and NSCC to the contraction by α1-adrenoceptor stimulation could be manipulated by increasing intracellular Ca2+ release from non-contractile sarcoplasmic reticulum Ca2+ stores. Results of this study point to a complex interactions between α1-adrenoceptor-mediated VSMC contractile performance and Ca2+ release form contractile or non-contractile Ca2+ stores with concomitant Ca2+ influx. Given the importance of VGCC and their blockers in arterial stiffening and hypertension, they further point toward an additional role of NSCC (and NSCC blockers) herein. 相似文献
6.
Ca2+ regulates cell differentiation and morphogenesis in a diversity of organisms and dysregulation of Ca2+ signal transduction pathways leads to many cellular pathologies. In Dictyostelium Ca2+ induces ecmB expression and stalk cell differentiation in vitro. Here we have analyzed the pattern of ecmB expression in intact and bisected slugs and the effect of agents that affect Ca2+ levels or antagonize calmodulin (CaM) on this expression pattern. We have shown that Ca2+ and CaM regulate ecmB expression and pstAB/pstB cell differentiation in vivo. Agents that increase intracellular Ca2+ levels increased ecmB expression and/or pstAB and pstB cell differentiation, while agents that decrease intracellular Ca2+ or antagonize CaM decreased it. In isolated slug tips agents that affect Ca2+ levels and antagonize CaM had differential effect on ecmB expression and cell differentiation in the anterior versus posterior zones. Agents that increase intracellular Ca2+ levels increased the number of ecmB expressing cells in the anterior region of slugs, while agents that decrease intracellular Ca2+ levels or antagonize CaM activity increased the number of ecmB expressing cells in the posterior. We have also demonstrated that agents that affect Ca2+ levels or antagonize CaM affect cells motility and regeneration of shape in isolated slug tips and backs and regeneration of tips in isolated slug backs. To our knowledge, this is the first study detailing the pattern of ecmB expression in regenerating slugs as well as the role of Ca2+ and CaM in the regeneration process and ecmB expression. 相似文献
7.
Shujiang Shang Changhe Wang Bin Liu Qihui WuQuanfeng Zhang Wei LiuLianghong Zheng Huadong XuXinjiang Kang Xiaoyu ZhangYeshi Wang Hui ZhengShirong Wang Wei Xiong Tao Liu Zhuan Zhou 《Cell calcium》2014
Classic calcium hypothesis states that depolarization-induced increase in intracellular Ca2+ concentration ([Ca2+]i) triggers vesicle exocytosis by increasing vesicle release probability in neurons and neuroendocrine cells. The extracellular Ca2+, in this calcium hypothesis, serves as a reservoir of Ca2+ source. Recently we find that extracellular Ca2+per se inhibits the [Ca2+]i dependent vesicle exocytosis, but it remains unclear whether quantal size is regulated by extracellular, or intracellular Ca2+ or both [1]. In this work we showed that, in physiological condition, extracellular Ca2+per se specifically inhibited the quantal size of single vesicle release in rat adrenal slice chromaffin cells. The extracellular Ca2+ in physiological concentration (2.5 mM) directly regulated fusion pore kinetics of spontaneous quantal release of catecholamine. In addition, removal of extracellular Ca2+ directly triggered vesicle exocytosis without eliciting intracellular Ca2+. We propose that intracellular Ca2+ and extracellular Ca2+per se cooperately regulate single vesicle exocytosis. The vesicle release probability was jointly modulated by both intracellular and extracellular Ca2+, while the vesicle quantal size was mainly determined by extracellular Ca2+ in chromaffin cells physiologically. 相似文献
8.
Marijke De Bock Elke Decrock Nan Wang Mélissa Bol Mathieu Vinken Geert Bultynck Luc Leybaert 《Biochimica et Biophysica Acta (BBA)/Molecular Cell Research》2014
For decades, studies have been focusing on the neuronal abnormalities that accompany neurodegenerative disorders. Yet, glial cells are emerging as important players in numerous neurological diseases. Astrocytes, the main type of glia in the central nervous system , form extensive networks that physically and functionally connect neuronal synapses with cerebral blood vessels. Normal brain functioning strictly depends on highly specialized cellular cross-talk between these different partners to which Ca2 +, as a signaling ion, largely contributes. Altered intracellular Ca2 + levels are associated with neurodegenerative disorders and play a crucial role in the glial responses to injury. Intracellular Ca2 + increases in single astrocytes can be propagated toward neighboring cells as intercellular Ca2 + waves, thereby recruiting a larger group of cells. Intercellular Ca2+ wave propagation depends on two, parallel, connexin (Cx) channel-based mechanisms: i) the diffusion of inositol 1,4,5-trisphosphate through gap junction channels that directly connect the cytoplasm of neighboring cells, and ii) the release of paracrine messengers such as glutamate and ATP through hemichannels (‘half of a gap junction channel’). This review gives an overview of the current knowledge on Cx-mediated Ca2 + communication among astrocytes as well as between astrocytes and other brain cell types in physiology and pathology, with a focus on the processes of neurodegeneration and reactive gliosis. Research on Cx-mediated astroglial Ca2 + communication may ultimately shed light on the development of targeted therapies for neurodegenerative disorders in which astrocytes participate. This article is part of a Special Issue entitled: Calcium signaling in health and disease. Guest Editors: Geert Bultynck, Jacques Haiech, Claus W. Heizmann, Joachim Krebs, and Marc Moreau. 相似文献
9.
Extracellular Calcium Sensing by Glial Cells: Low Extracellular Calcium Induces Intracellular Calcium Release and Intercellular Signaling 总被引:3,自引:0,他引:3
Abstract: Glial cells in primary mixed cultures or purified astrocyte cultures from mouse cortex respond to reduced extracellular calcium concentration ([Ca2+]e) with increases in intracellular calcium concentration ([Ca2+]i) that include single-cell Ca2+ oscillations and propagated intercellular Ca2+ waves. The rate and pattern of propagation of low [Ca2+]e-induced intercellular Ca2+ waves are altered by rapid perfusion of the extracellular medium, suggesting the involvement of an extracellular messenger in Ca2+ wave propagation. The low [Ca2+]e-induced Ca2+ response is abolished by thapsigargin and by the phospholipase antagonist U73122. The low [Ca2+]e-induced response is also blocked by replacement of extracellular Ca2+ with Ba2+, Zn2+, or Ni2+, and by 100 µM La3+. Glial cells in lowered [Ca2+]e(0.1–0.5 mM) show an increased [Ca2+]i response to bath application of ATP, whereas glial cells in increased [Ca2+]e (10–15 mM) show a decreased [Ca2+]i response to ATP. These results show that glial cells possess a mechanism for coupling between [Ca2+]e and the release of Ca2+ from intracellular stores. This mechanism may be involved in glial responses to the extracellular environment and may be important in pathological conditions associated with low extracellular Ca2+ such as seizures or ischemia. 相似文献
10.
Optical induction of muscle contraction at the tissue scale through intrinsic cellular amplifiers
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Jonghee Yoon Myunghwan Choi Taeyun Ku Won Jong Choi Chulhee Choi 《Journal of biophotonics》2014,7(8):597-606
The smooth muscle cell is the principal component responsible for involuntary control of visceral organs, including vascular tonicity, secretion, and sphincter regulation. It is known that the neurotransmitters released from nerve endings increase the intracellular Ca2+ level in smooth muscle cells followed by muscle contraction. We herein report that femtosecond laser pulses focused on the diffraction‐limited volume can induce intracellular Ca2+ increases in the irradiated smooth muscle cell without neurotransmitters, and locally increased intracellular Ca2+ levels are amplified by calcium‐induced calcium‐releasing mechanisms through the ryanodine receptor, a Ca2+ channel of the endoplasmic reticulum. The laser‐induced Ca2+ increases propagate to adjacent cells through gap junctions. Thus, ultrashort‐pulsed lasers can induce smooth muscle contraction by controlling Ca2+, even with optical stimulation of the diffraction‐limited volume. This optical method, which leads to reversible and reproducible muscle contraction, can be used in research into muscle dynamics, neuromuscular disease treatment, and nanorobot control. (© 2014 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim) 相似文献
11.
A. Verkhratsky 《Neurophysiology》1997,29(4-5):205-212
Various electrical, mechanical, and chemical stimuli, including the influences of neurotrasmitters, neuromodulators, and hormones,
trigger complex changes in [Ca2+]
i
in all types of glial cells. Glial [Ca2+]
i
responses are controlled by coordinated activity of several molecular cascades. The initiation of [Ca2+]
i
signal in glial cells results from activation of either plasmalemmal, or intracellular Ca2+ permeable channels. The interplay of different molecular cascades enables the development of agonist-specific patterns of
Ca2+ responses. Such agonist specificity may provide the means for intracellular and intercellular information coding. Furthermore,
glial [Ca2+]
i
signals can travel with no decrement within glial networks. These intercellular Ca2+ waves can be regarded as a substrate for information exchange between the glial cells. Neuronal activity can trigger [Ca2+]
i
signals in neighboring glial cells and, moreover, there is some evidence that glial [Ca2+]
i
waves can activate neuronal electrical and/or [Ca2+]
i
, responses. Glial Ca2+ signalling can be regarded as a form of glial excitability. 相似文献
12.
Simultaneous imaging of ER and cytosolic Ca2+ dynamics reveals long-distance ER Ca2+ waves in plants
Francesca Resentini Matteo Grenzi Daniele Ancora Mara Cademartori Laura Luoni Marianna Franco Andrea Bassi Maria Cristina Bonza Alex Costa 《Plant physiology》2021,187(2):603
Calcium ions (Ca2+) play a key role in cell signaling across organisms. In plants, a plethora of environmental and developmental stimuli induce specific Ca2+ increases in the cytosol as well as in different cellular compartments including the endoplasmic reticulum (ER). The ER represents an intracellular Ca2+ store that actively accumulates Ca2+ taken up from the cytosol. By exploiting state-of-the-art genetically encoded Ca2+ indicators, specifically the ER-GCaMP6-210 and R-GECO1, we report the generation and characterization of an Arabidopsis (Arabidopsis thaliana) line that allows for simultaneous imaging of Ca2+ dynamics in both the ER and cytosol at different spatial scales. By performing analyses in single cells, we precisely quantified (1) the time required by the ER to import Ca2+ from the cytosol into the lumen and (2) the time required to observe a cytosolic Ca2+ increase upon the pharmacological inhibition of the ER-localized P-Type IIA Ca2+-ATPases. Furthermore, live imaging of mature, soil-grown plants revealed the existence of a wounding-induced, long-distance ER Ca2+ wave propagating in injured and systemic rosette leaves. This technology enhances high-resolution analyses of intracellular Ca2+ dynamics at the cellular level and in adult organisms and paves the way to develop new methodologies aimed at defining the contribution of subcellular compartments in Ca2+ homeostasis and signaling.Dual color imaging allows the simultaneous analysis of calcium dynamics in the endoplasmic reticulum and cytosol from single cells to adult entire plants. 相似文献
13.
A. B. Uzdensky M. V. Rudkovskii G. M. Fedorenko E. V. Berezhnaya I. A. Ischenko V. D. Kovaleva M. A. Komandirov M. A. Neginskaya A. M. Khaitin S. A. Sharifulina 《Biochemistry (Moscow) Supplemental Series A: Membrane and Cell Biology》2014,8(1):1-15
Photodynamic therapy (PDT), an inducer of oxidative stress, is used for treatment of cancer, including brain tumors. To study the mechanisms of photodynamic injury of neurons and glial cells (GC), we used a simple model object — isolated crayfish mechanoreceptor consisting of a single sensory neuron surrounded by a multilayered glial envelope. PDT caused inhibition and elimination of neuronal activity, impairment of intracellular organelles involved in the biosynthetic, bioenergetic, and transport processes and neuroglial interactions, necrosis of neurons and glial cells, and in glial apoptosis. PDT-induced death of a neuron and GC was mediated by intercellular molecular messengers and intracellular signaling cascades. PDT-induced inhibition and elimination of neuronal activity was associated with opening of mitochondrial permeability transition pores, Ca2+ release into cytosol, protein kinase C and NO synthase activities. Necrosis of neurons was mediated by protein kinases B/Akt, GSK-3β and mTOR, opening of mitochondrial permeability transition pores and Ca2+/calmodulin/CaMKII pathway. NO and GDNF reduced neuronal necrosis. Multiple signal pathways, such as phospholipase C/Ca2+, Ca2+/calmodulin/CaMKII, Ca2+/PKC, Akt/mTOR, MEK/p38, and protein kinase G mediated PDT-induced necrosis both in glial cells and in neurons. NOS/NO and neurotrophic factors NGF and GDNF protected glial cells and demonstrated antinecrotic activity. Glial apoptosis was reduced by neurotrophic factors NGF and GDNF, protein kinase C, and MAP kinase JNK. In contrast, mitochondrial permeability transition pores and phospholipase C, which mobilize intracellular Ca2+, NOS/NO/protein kinase G, proteins GSK-3β and mTOR, stimulated apoptosis of glial cells. The schemes of involvement of various inter- and intracellular signaling processes in the responses of neurons and GC to PDT are developed. 相似文献
14.
Effective control of the Ca2+ homeostasis in any living cell is paramount to coordinate some of the most essential physiological processes, including cell division, morphological differentiation, and intercellular communication. Therefore, effective homeostatic mechanisms have evolved to maintain the intracellular Ca2+ concentration at physiologically adequate levels, as well as to regulate the spatial and temporal dynamics of Ca2+signaling at subcellular resolution. Members of the superfamily of EF-hand Ca2+-binding proteins are effective to either attenuate intracellular Ca2+ transients as stochiometric buffers or function as Ca2+ sensors whose conformational change upon Ca2+ binding triggers protein-protein interactions, leading to cell state-specific intracellular signaling events. In the central nervous system, some EF-hand Ca2+-binding proteins are restricted to specific subtypes of neurons or glia, with their expression under developmental and/or metabolic control. Therefore, Ca2+-binding proteins are widely used as molecular markers of cell identity whilst also predicting excitability and neurotransmitter release profiles in response to electrical stimuli. Secretagogin is a novel member of the group of EF-hand Ca2+-binding proteins whose expression precedes that of many other Ca2+-binding proteins in postmitotic, migratory neurons in the embryonic nervous system. Secretagogin expression persists during neurogenesis in the adult brain, yet becomes confined to regionalized subsets of differentiated neurons in the adult central and peripheral nervous and neuroendocrine systems. Secretagogin may be implicated in the control of neuronal turnover and differentiation, particularly since it is re-expressed in neoplastic brain and endocrine tumors and modulates cell proliferation in vitro. Alternatively, and since secretagogin can bind to SNARE proteins, it might function as a Ca2+ sensor/coincidence detector modulating vesicular exocytosis of neurotransmitters, neuropeptides or hormones. Thus, secretagogin emerges as a functionally multifaceted Ca2+-binding protein whose molecular characterization can unravel a new and fundamental dimension of Ca2+signaling under physiological and disease conditions in the nervous system and beyond. 相似文献
15.
Yuji Shono Masahiro Kamouchi Takanari Kitazono Junya Kuroda Kuniyuki Nakamura Noriko Hagiwara Hiroaki Ooboshi Setsuro Ibayashi Mitsuo Iida 《Cellular and molecular neurobiology》2010,30(3):453-460
Brain hypoxia or ischemia causes acidosis and the intracellular accumulation of Ca2+ in neuron. The aims of the present study were to elucidate the interaction between intracellular pH and Ca2+ during transient acidosis and its effects on the viability of neuronal and glial cells. Intracellular Ca2+ and pH were measured using the fluorescence of fura-2 and 2′,7′-bis(2-carboxyethyl)-5(6)-carboxyfluorescein acetoxymethyl
ester in neuroblastoma (IMR-32), glioblastoma (T98G), and astrocytoma (CCF-STTG1) cell lines. The administration of 5 mM propionate
caused intracellular acidification in IMR-32 and T98G cells but not in CCF-STTG1 cells. After the removal of propionate, the
intracellular pH recovered to the resting level. The intracellular Ca2+ transiently increased upon the removal of propionate in IMR-32 and T98G cells but not in CCF-STTG1 cells. The transient Ca2+ increase caused by the withdrawal of intracellular acidification was abolished by the removal of external Ca2+, diminished by a reduction of external Na+, and inhibited by benzamil. Transient acidosis caused cell death, whereas the cells were more viable in the absence of external
Ca2+. Benzamil alleviated cell death caused by transient acidosis in IMR-32 and T98G cells but not in CCF-STTG1 cells. These results
suggest that recovery from intracellular acidosis causes a transient increase in cytosolic Ca2+ due to reversal of Ca2+ transport via Na+/Ca2+ exchanger coactivated with Na+/H+ exchanger, which can cause cell death. 相似文献
16.
Yi Liu Vivienne Gianinazzi-Pearson Christine Arnould Daniel Wipf Bin Zhao Diederik van Tuinen 《Fungal biology》2013,117(1):22-31
Fluctuations in intracellular calcium levels generate signalling events and regulate different cellular processes. Whilst the implication of Ca2+ in plant responses during arbuscular mycorrhiza (AM) interactions is well documented, nothing is known about the regulation or role of this secondary messenger in the fungal symbiont. The spatio-temporal expression pattern of putatively Ca2+-related genes of Glomus intraradices BEG141 encoding five proteins involved in membrane transport and one nuclear protein kinase, was investigated during the AM symbiosis. Expression profiles related to successful colonization of host roots were observed in interactions of G. intraradices with roots of wild-type Medicago truncatula (line J5) compared to the mycorrhiza-defective mutant dmi3/Mtsym13. Symbiotic fungal activity was monitored using stearoyl-CoA desaturase and phosphate transporter genes. Laser microdissection based-mapping of fungal gene expression in mycorrhizal root tissues indicated that the Ca2+-related genes were differentially upregulated in arbuscules and/or in intercellular hyphae. The spatio-temporal variations in gene expression suggest that the encoded proteins may have different functions in fungal development or function during symbiosis development. Full-length cDNA obtained for two genes with interesting expression profiles confirmed a close similarity with an endoplasmic reticulum P-type ATPase and a Vcx1-like vacuolar Ca2+ ion transporter functionally characterized in other fungi and involved in the regulation of cell calcium pools. Possible mechanisms are discussed in which Ca2+-related proteins G. intraradices BEG141 may play a role in mobilization and perception of the intracellular messenger by the AM fungus during symbiotic interactions with host roots. 相似文献
17.
Robson Sartorello Maria Jimena Amaya Célia R.S. Garcia 《Biochemical and biophysical research communications》2009,389(4):586-592
Plasmodium falciparum, the most lethal malarial parasite, expresses an ortholog for the protein kinase C (PKC) activator RACK1. However, PKC has not been identified in this parasite, and the mammalian RACK1 can interact with the inositol 1,4,5-trisphosphate receptor (InsP3R). Therefore we investigated whether the Plasmodium ortholog PfRACK also can affect InsP3R-mediated Ca2+ signaling in mammalian cells. GFP-tagged PfRACK and endogenous RACK1 were expressed in a similar distribution within cells. PfRACK inhibited agonist-induced Ca2+ signals in cells expressing each isoform of the InsP3R, and this effect persisted when expression of endogenous RACK1 was reduced by siRNA. PfRACK also inhibited Ca2+ signals induced by photorelease of caged InsP3. These findings provide evidence that PfRACK directly inhibits InsP3-mediated Ca2+ signaling in mammalian cells. Interference with host cell signaling pathways to subvert the host intracellular milieu may be an important mechanism for parasite survival. 相似文献
18.
Plasmodium falciparum, the most important etiological agent of human malaria, is endowed with a highly complex cell cycle that is essential for
its successful replication within the host. A number of evidence suggest that changes in parasite Ca2+ levels occur during the intracellular cycle of the parasites and play a role in modulating its functions within the RBC.
However, the molecular identification of Plasmodium receptors linked with calcium signalling and the causal relationship between Ca2+ increases and parasite functions are still largely mysterious. We here describe that increases in P. falciparum Ca2+ levels, induced by extracellular ATP, modulate parasite invasion. In particular, we show that addition of ATP leads to an
increase of cytosolic Ca2+ in trophozoites and segmented schizonts. Addition of the compounds KN62 and Ip5I on parasites blocked the ATP-induced rise
in [Ca2+]c. Besides, the compounds or hydrolysis of ATP with apyrase added in culture drastically reduce RBC infection by parasites,
suggesting strongly a role of extracellular ATP during RBC invasion. The use of purinoceptor antagonists Ip5I and KN62 in
this study suggests the presence of putative purinoceptor in P. falciparum. In conclusion, we have demonstrated that increases in [Ca2+]c in the malarial parasite P. falciparum by ATP leads to the modulation of its invasion of red blood cells. 相似文献
19.
Glucose sensing mechanism has been intensively studied in pancreatic cells and neurons. Depolarization of membrane potential by closure of KATP , Kv and TASK channel, and subsequently Ca2+ entry via L-type voltage gated Ca2+ channel (VGCC) are implicated to mediate the signal transduction in these cells. However, the mechanism of non-excitable cells, which are lacking VGCC, for sensing glucose remains unclear. In this study, we utilized the calcium ratio measurement and patch clamping technique to study the effects of low glucose on [Ca2+]i and currents in the human embryonic kidney epithelial cells (HEK 293). We found low glucose evoked a significant reversible [Ca2+]i elevation in HEK 293 independent of the closure of Kv channels. This increase of [Ca2+]i was mediated by Ca2+ entry across plasma membrane and exhibited a dosage dependent behaviour to external glucose concentration. The low glucose-induced entry of Ca2+ was characterized as a voltage independent behaviour and had cation permeability to Na+ and Ca2+. The modulation of PLC, AMPK, tyrosine kinase and cADPribose failed to regulate this glucose-sensitive Ca2+ entry. In addition, the entry of Ca2+ was insensitive to nifedipine, 2APB, SKF, La3+, Gd3+, and KBR9743, suggesting a novel signal pathway in mediating glucose sensing. 相似文献