共查询到20条相似文献,搜索用时 31 毫秒
1.
Background
Although various endothelium-dependent relaxing factors (endothelial autacoids) are released upon the elevation of endothelial cytosolic free Ca2+ concentration (EC [Ca2+]i), the quantitative relationship between EC [Ca2+]i and vascular tone remains to be established. Moreover, whether the basal release of endothelial autacoids is modulated by basal EC [Ca2+]i is still unclear. We assessed these issues by using a novel method that allows simultaneous recording of EC [Ca2+]i and vascular displacement in dissected rat aortic segments. 相似文献2.
Subtypes of purinergic receptors involved in modulation of cytoplasmic calcium ion concentration ([Ca2+]i) and insulin release in mouse pancreatic β-cells were examined in two systems, pancreatic islets in primary culture and beta-TC6
insulinoma cells. Both systems exhibited some physiological responses such as acetylcholine-stimulated [Ca2+]i rise via cytoplasmic Ca2+ mobilization. Addition of ATP, ADP, and 2-MeSADP (each 100 μM) transiently increased [Ca2+]i in single islets cultured in the presence of 5.5 mM (normal) glucose. The potent P2Y1 receptor agonist 2-MeSADP reduced insulin secretion significantly in islets cultured in the presence of high glucose (16.7 mM),
whereas a slight stimulation occurred at 5.5 mM glucose. The selective P2Y6 receptor agonist UDP (200 μM) transiently increased [Ca2+]i and reduced insulin secretion at high glucose, whereas the P2Y2/4 receptor agonist UTP and adenosine receptor agonist NECA were inactive. [Ca2+]i transients induced by 2-MeSADP and UDP were antagonized by suramin (100 μM), U73122 (2 μM, PLC inhibitor), and 2-APB (10
or 30 μM, IP3 receptor antagonist), but neither by staurosporine (1 μM, PKC inhibitor) nor depletion of extracellular Ca2+. The effect of 2-MeSADP on [Ca2+]i was also significantly inhibited by MRS2500, a P2Y1 receptor antagonist. These results suggested that P2Y1 and P2Y6 receptor subtypes are involved in Ca2+ mobilization from intracellular stores and insulin release in mouse islets. In beta-TC6 cells, ATP, ADP, 2-MeSADP, and UDP
transiently elevated [Ca2+]i and slightly decreased insulin secretion at normal glucose, while UTP and NECA were inactive. RT-PCR analysis detected mRNAs
of P2Y1 and P2Y6, but not P2Y2 and P2Y4 receptors. 相似文献
3.
Schaloske RH Lusche DF Bezares-Roder K Happle K Malchow D Schlatterer C 《BMC cell biology》2005,6(1):13
Background
Stimulation of Dictyostelium discoideum with cAMP evokes an elevation of the cytosolic free Ca2+ concentration ([Ca2+]i). The [Ca2+]i-change is composed of liberation of stored Ca2+ and extracellular Ca2+-entry. The significance of the [Ca2+]i-transient for chemotaxis is under debate. Abolition of chemotactic orientation and migration by Ca2+-buffers in the cytosol indicates that a [Ca2+]i-increase is required for chemotaxis. Yet, the iplA - mutant disrupted in a gene bearing similarity to IP3-receptors of higher eukaryotes aggregates despite the absence of a cAMP-induced [Ca2+]i-transient which favours the view that [Ca2+]i-changes are insignificant for chemotaxis. 相似文献4.
Summary Discrepancies about the role of L-type voltage-gated calcium channels (VGCC) in acetylcholine (ACh)-induced [Ca2+]i oscillations in tracheal smooth muscle cells (TSMCs) have been seen in recent reports. We demonstrate here that ACh-induced
[Ca2+]i oscillations in TMCS were reversibly inhibited by three VGCC blockers, nicardipine, nifedipine and verapamil. Prolonged (several
minutes) application of VGCC blockers, led to tachyphylaxis; that is, [Ca2+]i oscillations resumed, but at a lower frequency. Brief (15–30 s) removal of VGCC blockers re-sensitized [Ca2+]i oscillations to inhibition by the agents. Calcium oscillations tolerant to VGCC blockers were abolished by KB-R7943, an inhibitor
of the reverse mode of Na+/Ca2+ exchanger (NCX). KB-R7943 alone also abolished ACh-induced [Ca2+]i oscillations. Enhancement of the reverse mode of NCX via removing extracellular Na+ reversed inhibition of ACh-induced [Ca2+]i oscillations by VGCC blockers. Inhibition of non-selective cation channels using Gd3+ slightly reduced the frequency of ACh-induced [Ca2+]i oscillations, but did not prevent the occurrence of tachyphylaxis. Altogether, these results suggest that VGCC and the reverse
mode of NCX are two primary Ca2+ entry pathways for maintaining ACh-induced [Ca2+]i oscillations in TSMCs. The two pathways complement each other, and may account for tachyphylaxis of ACh-induced [Ca2+]i oscillations to VGCC blockers. 相似文献
5.
The effect of ANG II on pHi, [Ca2+]i and cell volume was investigated in T84 cells, a cell line originated from colon epithelium, using the probes BCECF-AM, Fluo
4-AM and acridine orange, respectively. The recovery rate of pHi via the Na+/H+ exchanger was examined in the first 2 min following the acidification of pHi with a NH4Cl pulse. In the control situation, the pHi recovery rate was 0.118 ± 0.001 (n = 52) pH units/min and ANG II (10−12 M or 10−9 M) increased this value (by 106% or 32%, respectively) but ANG II (10−7 M) decreased it to 47%. The control [Ca2+]i was 99 ± 4 (n = 45) nM and ANG II increased this value in a dose-dependent manner. The ANG II effects on cell volume were minor and late
and should not interfere in the measurements of pHi recovery and [Ca2+]i. To document the signaling pathways in the hormonal effects we used: Staurosporine (a PKC inhibitor), W13 (a calcium-dependent
calmodulin antagonist), H89 (a PKA inhibitor) or Econazole (an inhibitor of cytochrome P450 epoxygenase). Our results indicate
that the biphasic effect of ANG II on Na+/H+ exchanger is a cAMP-independent mechanism and is the result of: 1) stimulation of the exchanger by PKC signaling pathway
activation (at 10−12 – 10−7 M ANG II) and by increases of [Ca2+]i in the lower range (at 10−12 M ANG II) and 2) inhibition of the exchanger at high [Ca2+]i levels (at 10−9 – 10−7 M ANG II) through cytochrome P450 epoxygenase-dependent metabolites of the arachidonic acid signaling pathway. 相似文献
6.
Our previous results have demonstrated that both nitric oxide (NO) and hydrogen peroxide (H2O2) are involved in the promotion of adventitious root development in marigold (Tagetes erecta L.). However, not much is known about the intricate molecular network of adventitious root development triggered by NO and
H2O2. In this study, the involvement of calcium (Ca2+) and calmodulin (CaM) in NO- and H2O2-induced adventitious rooting in marigold was investigated. Exogenous Ca2+ was capable of promoting adventitious rooting, with a maximal biological response at 50 μM CaCl2. Ca2+ chelators and CaM antagonists prevented NO- and H2O2-induced adventitious rooting, indicating that both endogenous Ca2+ and CaM may play crucial roles in the adventitious rooting induced by NO and H2O2. NO and H2O2 treatments increased the endogenous content of Ca2+ and CaM, suggesting that NO and H2O2 enhanced adventitious rooting by stimulating the endogenous Ca2+ and CaM levels. Moreover, treatment with Ca2+ enhanced the endogenous levels of NO and H2O2. Additionally, Ca2+ might be involved as an upstream signaling molecule for CaM during NO- and H2O2-induced rooting. Altogether, the results suggest that both Ca2+ and CaM are two downstream signaling molecules in adventitious rooting induced by NO and H2O2. 相似文献
7.
Preload-induced changes of active tension and [Ca2+]i are “dissociated” in mammalian myocardium. This study aimed to describe the distinct effects of preload at low and physiological
[Ca2+]o. Rat RV papillary muscles were studied in isometric conditions at 25‡C and 0.33 Hz at 1 mM (hypo-Ca group) and 2.5 mM [Ca2+]o (normal-Ca group). [Ca2+]i was monitored with fura-2/AM. Increase of preload caused a rise of active tension in hypo-Ca and normal-Ca groups whereas
peak fluorescence rose significantly only at low [Ca2+]o. End-diastolic tension, end-diastolic level of fluorescence, time-to-peak tension, but not time-to-peak of Ca2+ transient, progressively increased with preload. Mechanical relaxation decelerated with preload while Ca2+ transient decay time decreased in the initial phase and increased in the late phase, resulting in a prominent “bump” configuration.
The “bump” was assessed as a ratio of its area to the fluorescence trace area. It was a new finding that the preload-induced
rise of this ratio was twice as large in hypo-Ca. Our results indicate that preload-induced changes in active tension and
[Ca2+]i are “dissociated” in rat myocardium, with relatively higher expression at low [Ca2+]o. Ca-dependence of Ca-TnC association/dissociation kinetics is thought to be a main contributor to these preload-induced effects. 相似文献
8.
Bjaelde RG Arnadottir SS Leipziger J Praetorius HA 《The Journal of membrane biology》2011,244(1):43-53
Translocation of vesicles within the cytoplasm is essential to normal cell function. The vesicles are typically transported
along the microtubules to their destination. The aim of this study was to characterize the vesicular movement in resting and
stimulated renal epithelial cells. MDCK cells loaded with either quinacrine or acridine orange, dyes taken up by acidic vesicles,
were observed at 37°C in semiopen perfusion chambers. Time-lapse series were analyzed by Imaris software. Our data revealed
vigorous movement of stained vesicles in resting MDCK cells. These movements seem to require intact microtubules because nocodazole
leads to a considerable reduction of the vesicular movements. Interestingly, we found that extracellular ATP caused the vesicular
movement to cease. This observation was obvious in time lapse. Similarly, other stimuli known to increase the intracellular
Ca2+ concentration ([Ca2+]i) in MDCK cells (increment in the fluid flow rate or arginine vasopressin) also reduced the vesicular movement. These findings
were quantified by analysis of single vesicular movement patterns. In this way, ATP was found to reduce the lateral displacement
of the total population of vesicles by 40%. Because all these perturbations increase [Ca2+]i, we speculated that this increase in [Ca2+]i was responsible for the vesicle arrest. Therefore, we tested the effect of the Ca2+ ionophore, ionomycin (1 μM), which in the presence of extracellular Ca2+ resulted in a considerable and sustained reduction of vesicular movement amounting to a 58% decrease in average lateral vesicular
displacement. Our data suggest that vesicles transported on microtubules are paused when subjected to high intracellular Ca2+ concentrations. This may provide an additional explanation for the cytotoxic effect of high [Ca2+]i. 相似文献
9.
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
10.
Craviso GL Choe S Chatterjee P Chatterjee I Vernier PT 《Cellular and molecular neurobiology》2010,30(8):1259-1265
Exposing bovine chromaffin cells to a single 5 ns, high-voltage (5 MV/m) electric pulse stimulates Ca2+ entry into the cells via L-type voltage-gated Ca2+ channels (VGCC), resulting in the release of catecholamine. In this study, fluorescence imaging was used to monitor nanosecond
pulse-induced effects on intracellular Ca2+ level ([Ca2+]i) to investigate the contribution of other types of VGCCs expressed in these cells in mediating Ca2+ entry. ω-Conotoxin GVIA and ω-agatoxin IVA, antagonists of N-type and P/Q-type VGCCs, respectively, reduced the magnitude
of the rise in [Ca2+]i elicited by a 5 ns pulse. ω-conotoxin MVIIC, which blocks N- and P/Q-type VGCCs, had a similar effect. Blocking L-, N-, and
P\Q-type channels simultaneously with a cocktail of VGCC inhibitors abolished the pulse-induced [Ca2+]i response of the cells, suggesting Ca2+ influx occurs only via VGCCs. Lowering extracellular K+ concentration from 5 to 2 mM or pulsing cells in Na+-free medium suppressed the pulse-induced rise in [Ca2+]i in the majority of cells. Thus, both membrane potential and Na+ entry appear to play a role in the mechanism by which nanoelectropulses evoke Ca2+ influx. However, activation of voltage-gated Na+ channels (VGSC) is not involved since tetrodotoxin (TTX) failed to block the pulse-induced rise in [Ca2+]i. These findings demonstrate that a single electric pulse of only 5 ns duration serves as a novel stimulus to open multiple
types of VGCCs in chromaffin cells in a manner involving Na+ transport across the plasma membrane. Whether Na+ transport occurs via non-selective cation channels and/or through lipid nanopores remains to be determined. 相似文献
11.
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
12.
Intracellular calcium ([Ca2+]i) plays a pivotal role in neuronal ischemia. The aim of the present study was to investigate the routes of Ca2+ entry during non-excitotoxic oxygen and glucose deprivation (OGD) in acutely dissociated rat CA1 neurons. During OGD the fluo-3/fura red ratio reflecting [Ca2+]i increased rapidly and irreversibly. [Ca2+]i increased to the same degree in Ca2+ depleted medium, and also when both the ryanodine receptors (RyR) and the inositol 1,4,5-trisphosphate (IP3) receptors were blocked. When the endoplasmic reticulum (ER) Ca2+ stores were emptied with thapsigargin no increase in [Ca2+]i was observed independent of extracellular Ca2+. The OGD induced Ca2+ deregulation in isolated CA1 neurons is not prevented by removing Ca2+, or by blocking the IP3– or RyR receptors. However, when SERCA was blocked, no increase in [Ca2+]i was observed suggesting that SERCA dysfunction represents an important mechanism for ischemic Ca2+ overload. 相似文献
13.
Background
Differentiating Dictyostelium discoideum amoebae respond upon cAMP-stimulation with an increase in the cytosolic free Ca2+ concentration ([Ca2+]i) that is composed of liberation of stored Ca2+ and extracellular Ca2+-influx. In this study we investigated whether intracellular cAMP is involved in the control of [Ca2+]i. 相似文献14.
Gang Tang Yi Shen Pan Gao Shuang-Shuang Song Liang-Yi Si 《In vitro cellular & developmental biology. Animal》2018,54(3):250-256
Cardiac hypertrophy plays a major role in heart failure and is related to patient morbidity and mortality. Calcium overloading is a main risk for cardiac hypertrophy, and Na+/K+-ATPase (NKA) has been found that it could not only regulate intracellular Na+ levels but also control the intracellular Ca2+ ([Ca2+]i) level through Na+/Ca2+-exchanger (NCX). Recent studies have reported that klotho could affect [Ca2+]i level. In this study, we aimed at exploring the role of klotho in improving isoproterenol-induced hypertrophic response of H9C2 cells. The H9C2 cells were randomly divided into control and isoproterenol (ISO) (10 μM) groups. Klotho protein (10 μg/ml) or NKAα2 siRNA was used to determine the changes in isoproterenol-induced hypertrophic response. The alterations of [Ca2+]i level were measured by spectrofluorometry. Our results showed that H9C2 cells which were treated with isoproterenol presented a higher level of [Ca2+]i and hypertrophic gene expression at 24 and 48 h compared with the control group. Moreover, the expressions of NKAα1 and NKAα2 were both increased in control and ISO groups after treating with klotho protein; meanwhile, the NKA activity was increased and NCX activity was decreased after treatment. Consistently, the [Ca2+]i level and hypertrophic gene expression were decreased in ISO group after klotho protein treatment. However, these effects were both prevented by transfecting with NKAα2 siRNA. In conclusion, these findings demonstrated that klotho inhibits isoproterenol-induced hypertrophic response in H9C2 cells by activating NKA and inhibiting the reverse mode of NCX and this effect may be associated with the upregulation of NKAα2 expression. 相似文献
15.
Liu J Wang F Huang C Long LH Wu WN Cai F Wang JH Ma LQ Chen JG 《Cellular and molecular neurobiology》2009,29(3):317-328
Recent evidences indicate the existence of an atypical D1 dopamine receptor other than traditional D1 dopamine receptor in the brain that mediates PI hydrolysis via activation of phospholipase Cβ (PLCβ). To further understand the basic physiological function of this receptor in brain, the effects of a selective phosphoinositide
(PI)-linked D1 dopamine receptor agonist SKF83959 on cytosolic free calcium concentration ([Ca2+]i) in cultured rat prefrontal cortical astrocytes were investigated by calcium imaging. The results indicated that SKF83959
caused a transient dose-dependent increase in [Ca2+]i. Application of D1 receptor, but not D2, α1 adrenergic, 5-HT receptor, or cholinergic antagonist prevented SKF83959-induced [Ca2+]i rise, indicating that activation of the D1 dopamine receptor was essential for this response. Increase in [Ca2+]i was a two-step process characterized by an initial increase in [Ca2+]i mediated by release from intracellular stores, supplemented by influx through voltage-gated calcium channels, receptor-operated
calcium channels, and capacitative Ca2+ entry. Furthermore, SKF83959-stimulated increase in [Ca2+]i was abolished following treatment with a PLC inhibitor. Overall, these results suggested that activation of D1 receptor by SKF83959 mediates a dose-dependent mobilization of [Ca2+]i via the PLC signaling pathway in cultured rat prefrontal cortical astrocytes. 相似文献
16.
E. A. Turovskii M. V. Konakov A. V. Berezhnov V. P. Zinchenko G. E. Bronnikov L. P. Dolgacheva 《Cell and Tissue Biology》2011,5(5):511-519
The thermogenic capability of brown adipose tissue is controlled by noradrenaline. By interacting with α1- and β-adrenoreceptors
of adipocytes, noradrenaline (NA) increases the intracellular concentration of Ca2+ ([Ca2+]i) and cAMP. The changes in [Ca2+]i under the action of NA and selective agonists of α1- and β-adrenoreceptors, i.e., cirazoline and isoproterenol (IP), are
recorded on individual cells of the primary culture of adipocytes during the day in vitro (DIV) 1, DIV 3, and DIV 6. The change
in [Ca2+]i under the effect of IP as compared to the response to cirazoline in cells of DIV 1 is characterized by a higher amplitude
and shorter duration of impulses in the entire diapason of the used physiological concentrations. After DIV 3, these differences
are insignificant and, after DIV 6, the differences in kinetics are nearly absent. For all three agonists, the kinetics of
the [Ca2+]i change in the proliferating and differentiated cells is significantly different; i.e., the response amplitude increases with
the age of the culture and the duration of transitory response decreases, while sensitivity to agonists of adrenoreceptors
increases. It can be seen from the rise in [Ca2+]i with an inhibitor of Ca2+-ATPase of the endoplasmic reticulum thapsigargin in calcium-free medium that the source of calcium ions in the endoplasmic
reticulum rises with the growth and development of cells in culture, while the rate at which Ca2+ is pumped out of cells, which characterizes the activity of Ca2+-ATPase of the plasma membrane, increases. 相似文献
17.
Yun-Bo Guo Ya Wen Wen-Xue Gao Jing-Chao Li Peng Zhou Zai-Ling Bai Bo Zhang Shi-Qiang Wang 《生物学前沿》2010,5(4):369-377
In dividing embryos, a localized elevation in intracellular Ca2+ ([Ca2+]i) at the cleavage furrow has been shown to be essential for cytokinesis. However, the underlying mechanisms for generating
and maintaining these [Ca2+]i gradients throughout cytokinesis are not fully understood. In the present study, we analyzed the role of inositol 1,4,5-trisphosphate
receptors (IP3Rs) and endoplasmic reticulum (ER) distribution in determining the intracellular Ca2+ gradients in early zebrafish blastomeres. Application of the injected Ca2+ indicator, Indo-1, showed that during the first cell division a standing Ca2+ gradient was formed ∼35 min after fertilization, with the [Ca2+]i spatially decaying from 500–600 nmol/L at the cleavage furrow to 100–200 nmol/L around the nucleus. While the IP3R immunohistochemical
fluorescence was relatively concentrated in the peri-furrow region, ER labeling was relatively enriched in both peri-furrow
and peri-nuclear regions. Numeric simulation suggested that a divergence in the spatial distribution of IP3R and the locations
of Ca2+ uptake within the ER was essential for the formation of a standing Ca2+ gradient, and the Ca2+ gradient could only be well-established under an optimal stoichiometry of Ca2+ uptake and release. Indeed, while inhibition of IP3R Ca2+ release blocked the generation of the Ca2+ gradient at a lower [Ca2+]i level, both Ca2+ release stimulation by inositol 1,4,5-trisphosphate (IP3) injection and ER Ca2+ pump inhibition by cyclopiazonic acid also eliminated the Ca2+ gradients at higher [Ca2+]i levels. Our results suggest a dynamic relationship between ER-mediated Ca2+ release and uptake that underlies the maintenance of the perifurrow Ca2+ gradient and is essential for cytokinesis of zebrafish embryos. 相似文献
18.
Gonzalez A Santofimia-Castaño P Rivera-Barreno R Salido GM 《Journal of physiology and biochemistry》2012,68(2):181-191
This work was designed in order to gain an insight on the mechanisms by which antioxidants prevent pancreatic disorders. We
have examined the properties of cinnamtannin B-1, which belongs to the class of polyphenols, against the effect of hydrogen
peroxide (H2O2) in mouse pancreatic acinar cells. We have studied Ca2+ mobilization, oxidative state, amylase secretion, and cell viability of cells treated with cinnamtannin B-1 in the presence
of various concentrations of H2O2. We found that H2O2 (0.1–100 μM) increased CM-H2DCFDA-derived fluorescence, reflecting an increase in oxidation. Cinnamtannin B-1 (10 μM) reduced H2O2-induced oxidation of CM-H2DCFDA. CCK-8 induced oxidation of CM-H2DCFDA in a similar way to low micromolar concentrations of H2O2, and cinnamtannin B-1 reduced the oxidant effect of CCK-8. In addition, H2O2 induced a slow and progressive increase in intracellular free Ca2+ concentration ([Ca2+]c). Cinnamtannin B-1 reduced the effect of H2O2 on [Ca2+]c, but only at the lower concentrations of the oxidant. H2O2 inhibited amylase secretion in response to cholecystokinin, and cinnamtannin B-1 reduced the inhibitory action of H2O2 on enzyme secretion. Finally, H2O2 reduced cell viability, and the antioxidant protected acinar cells against H2O2. In conclusion, the beneficial effects of cinnamtannin B-1 appear to be mediated by reducing the intracellular Ca2+ overload and intracellular accumulation of digestive enzymes evoked by ROS, which is a common pathological precursor that
mediates pancreatitis. Our results support the beneficial effect of natural antioxidants in the therapy against oxidative
stress-derived deleterious effects on cellular physiology. 相似文献
19.
Yuqing Wang Yingfang Zhu Yu Ling Haiyan Zhang Peng Liu František Baluška Jozef Šamaj Jinxing Lin Qinli Wang 《BMC plant biology》2010,10(1):53
Background
Mitochondria are dynamic organelles that move along actin filaments, and serve as calcium stores in plant cells. The positioning and dynamics of mitochondria depend on membrane-cytoskeleton interactions, but it is not clear whether microfilament cytoskeleton has a direct effect on mitochondrial function and Ca2+ storage. Therefore, we designed a series of experiments to clarify the effects of actin filaments on mitochondrial Ca2+ storage, cytoplasmic Ca2+ concentration ([Ca2+]c), and the interaction between mitochondrial Ca2+ and cytoplasmic Ca2+ in Arabidopsis root hairs. 相似文献20.
Salinity is among the environmental factors that affect plant growth and development and constrain agricultural productivity. Salinity stress triggers increases in cytosolic free Ca2+ concentration ([Ca2+]i) via Ca2+ influx across the plasma membrane. Salinity stress, as well as other stresses, induces the production of reactive oxygen species (ROS). It is well established that ROS also triggers increases in [Ca2+]i. However, the relationship and interaction between salinity stress-induced [Ca2+]i increases and ROS-induced [Ca2+]i increases remain poorly understood. Using an aequorin-based Ca2+ imaging assay we have analyzed [Ca2+]i changes in response to NaCl and H2O2 treatments in Arabidopsis thaliana. We found that NaCl and H2O2 together induced larger increases in [Ca2+]i in Arabidopsis seedlings than either NaCl or H2O2 alone, suggesting an additive effect on [Ca2+]i increases. Following a pre-treatment with either NaCl or H2O2, the subsequent elevation of [Ca2+]i in response to a second treatment with either NaCl or H2O2 was significantly reduced. Furthermore, the NaCl pre-treatment suppressed the elevation of [Ca2+]i seen with a second NaCl treatment more than that seen with a second treatment of H2O2. A similar response was seen when the initial treatment was with H2O2; subsequent addition of H2O2 led to less of an increase in [Ca2+]i than did addition of NaCl. These results imply that NaCl-gated Ca2+ channels and H2O2-gated Ca2+ channels may differ, and also suggest that NaCl- and H2O2-evoked [Ca2+]i may reduce the potency of both NaCl and H2O2 in triggering [Ca2+]i increases, highlighting a feedback mechanism. Alternatively, NaCl and H2O2 may activate the same Ca2+ permeable channel, which is expressed in different types of cells and/or activated via different signaling pathways. 相似文献