Journal articles: 'Intracellular calcium homeostasis'

1

Carafoli, E. "Intracellular Calcium Homeostasis." Annual Review of Biochemistry 56, no. 1 (June 1987): 395–433. http://dx.doi.org/10.1146/annurev.bi.56.070187.002143.

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Nicholls, D. G. "INTRACELLULAR CALCIUM HOMEOSTASIS." British Medical Bulletin 42, no. 4 (1986): 353–58. http://dx.doi.org/10.1093/oxfordjournals.bmb.a072152.

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Bronner, Felix. "Extracellular and Intracellular Regulation of Calcium Homeostasis." Scientific World JOURNAL 1 (2001): 919–25. http://dx.doi.org/10.1100/tsw.2001.489.

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An organism with an internal skeleton must accumulate calcium while maintaining body fluids at a well-regulated, constant calcium concentration. Neither calcium absorption nor excretion plays a significant regulatory role. Instead, isoionic calcium uptake and release by bone surfaces causes plasma calcium to be well regulated. Very rapid shape changes of osteoblasts and osteoclasts, in response to hormonal signals, modulate the available bone surfaces so that plasma calcium can increase when more low-affinity bone calcium binding sites are made available and can decrease when more high-affinity binding sites are exposed. The intracellular free calcium concentration of body cells is also regulated, but because cells are bathed by fluids with vastly higher calcium concentration, their major regulatory mechanism is severe entry restriction. All cells have a calcium-sensing receptor that modulates cell function via its response to extracellular calcium. In duodenal cells, the apical calcium entry structure functions as both transporter and a vitamin D–responsive channel. The channel upregulates calcium entry, with intracellular transport mediated by the mobile, vitamin D–dependent buffer, calbindin D9K, which binds and transports more than 90% of the transcellular calcium flux. Fixed intracellular calcium binding sites can, like the body's skeleton, take up and release calcium that has entered the cell, but the principal regulatory tool of the cell is restricted entry.

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Barry, W. H., and J. H. Bridge. "Intracellular calcium homeostasis in cardiac myocytes." Circulation 87, no. 6 (June 1993): 1806–15. http://dx.doi.org/10.1161/01.cir.87.6.1806.

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Shapiro, Steven M., Severn B. Churn, Shubro Pal, David Limbrick, and Robert J. DeLorenzo. "Bilirubin Alters Intracellular Calcium Homeostasis • 1135." Pediatric Research 43 (April 1998): 195. http://dx.doi.org/10.1203/00006450-199804001-01156.

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VERKHRATSKY, ALEXEJ, RICHARD K. ORKAND, and HELMUT KETTENMANN. "Glial Calcium: Homeostasis and Signaling Function." Physiological Reviews 78, no. 1 (January 1, 1998): 99–141. http://dx.doi.org/10.1152/physrev.1998.78.1.99.

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Verkhratsky, Alexej, Richard K. Orkand, and Helmut Kettenmann. Glial Calcium: Homeostasis and Signaling Function. Physiol. Rev. 78: 99–141, 1998. — Glial cells respond to various electrical, mechanical, and chemical stimuli, including neurotransmitters, neuromodulators, and hormones, with an increase in intracellular Ca2+ concentration ([Ca2+]i). The increases exhibit a variety of temporal and spatial patterns. These [Ca2+]i responses result from the coordinated activity of a number of molecular cascades responsible for Ca2+ movement into or out of the cytoplasm either by way of the extracellular space or intracellular stores. Transplasmalemmal Ca2+ movements may be controlled by several types of voltage- and ligand-gated Ca2+-permeable channels as well as Ca2+ pumps and a Na+/Ca2+ exchanger. In addition, glial cells express various metabotropic receptors coupled to intracellular Ca2+ stores through the intracellular messenger inositol 1,4,5-trisphosphate. The interplay of different molecular cascades enables the development of agonist-specific patterns of Ca2+ responses. Such agonist specificity may provide a means for intracellular and intercellular information coding. Calcium signals can traverse gap junctions between glial cells without decrement. These waves can serve as a substrate for integration of glial activity. By controlling gap junction conductance, Ca2+ waves may define the limits of functional glial networks. Neuronal activity can trigger [Ca2+]i signals in apposed glial cells, and moreover, there is some evidence that glial [Ca2+]i waves can affect neurons. Glial Ca2+ signaling can be regarded as a form of glial excitability.

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De Flora, A., U. Benatti, L. Guida, G. Forteleoni, and T. Meloni. "Favism: disordered erythrocyte calcium homeostasis." Blood 66, no. 2 (August 1, 1985): 294–97. http://dx.doi.org/10.1182/blood.v66.2.294.294.

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Abstract The biochemical events that take place during acute hemolysis of G6PD- deficient subjects in favism are far from being elucidated. Evidence is here reported for a constantly and heavily disordered calcium homeostasis in the erythrocytes from seven favic patients. The abnormality, ie, a significantly impaired calcium ATPase activity and a parallel marked increase of intracellular calcium levels, was characteristic of the acute hemolytic crisis although unrelated to the attendant reticulocytosis. Concomitantly, a remarkable decrease of intracellular potassium was also observed. The mean +/- SD Ca2+-ATPase activity in the favic patients was 20.8 +/- 7.8 mumol Pi/g Hb/h compared with 37.2 +/- 8.5 in the matched controls represented by 12 healthy G6PD-deficient subjects (P less than .001). The mean +/- SD intraerythrocytic calcium content was 288 +/- 158 mumol/L of erythrocytes in the favic patients as compared with 22.0 +/- 8.2 in the G6PD-deficient controls (P less than .001). The intraerythrocytic potassium content was 76.6 +/- 19.3 mmol/L of erythrocytes in the favic patients and 106.6 +/- 8.2 in the G6PD-deficient controls (P less than .001). In vitro incubation of normal and G6PD-deficient erythrocytes with divicine, a pyrimidine aglycone present in fava beans and strongly implicated in the pathogenesis of favism, reproduces most of these events, including drop of calcium ATPase, increased intracellular calcium, and leakage of erythrocyte potassium.

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De Flora, A., U. Benatti, L. Guida, G. Forteleoni, and T. Meloni. "Favism: disordered erythrocyte calcium homeostasis." Blood 66, no. 2 (August 1, 1985): 294–97. http://dx.doi.org/10.1182/blood.v66.2.294.bloodjournal662294.

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The biochemical events that take place during acute hemolysis of G6PD- deficient subjects in favism are far from being elucidated. Evidence is here reported for a constantly and heavily disordered calcium homeostasis in the erythrocytes from seven favic patients. The abnormality, ie, a significantly impaired calcium ATPase activity and a parallel marked increase of intracellular calcium levels, was characteristic of the acute hemolytic crisis although unrelated to the attendant reticulocytosis. Concomitantly, a remarkable decrease of intracellular potassium was also observed. The mean +/- SD Ca2+-ATPase activity in the favic patients was 20.8 +/- 7.8 mumol Pi/g Hb/h compared with 37.2 +/- 8.5 in the matched controls represented by 12 healthy G6PD-deficient subjects (P less than .001). The mean +/- SD intraerythrocytic calcium content was 288 +/- 158 mumol/L of erythrocytes in the favic patients as compared with 22.0 +/- 8.2 in the G6PD-deficient controls (P less than .001). The intraerythrocytic potassium content was 76.6 +/- 19.3 mmol/L of erythrocytes in the favic patients and 106.6 +/- 8.2 in the G6PD-deficient controls (P less than .001). In vitro incubation of normal and G6PD-deficient erythrocytes with divicine, a pyrimidine aglycone present in fava beans and strongly implicated in the pathogenesis of favism, reproduces most of these events, including drop of calcium ATPase, increased intracellular calcium, and leakage of erythrocyte potassium.

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9

CARAFOLI, ERNESTO. "The Intracellular Homeostasis of Calcium: An Overview." Annals of the New York Academy of Sciences 551, no. 1 Membrane in C (December 1988): 147–57. http://dx.doi.org/10.1111/j.1749-6632.1988.tb22333.x.

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Gandolfi, Luisella, Maria Pia Stella, Pamela Zambenedetti, and Paolo Zatta. "Aluminum alters intracellular calcium homeostasis in vitro." Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 1406, no. 3 (April 1998): 315–20. http://dx.doi.org/10.1016/s0925-4439(98)00018-0.

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Oz, Helieh S., Murray Wittner, Herbert B. Tanowitz, John P. Bilezikian, Maya Saxon, and Stephen A. Morris. "Trypanosoma cruzi: Mechanisms of intracellular calcium homeostasis." Experimental Parasitology 74, no. 4 (June 1992): 390–99. http://dx.doi.org/10.1016/0014-4894(92)90201-k.

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Кайрат, Б. К., С. Т. Тулеуханов, and В. П. Зинченко. "FEATURES OF CALCIUM HOMEOSTASIS AND CALCIUM SIGNALING IN NEURONS." Vestnik, no. 1 (June 17, 2021): 208–14. http://dx.doi.org/10.53065/kaznmu.2021.95.99.044.

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Ионы Са являются основным мессенджером в регуляции физиологических функций клеток. Внутриклеточном пространстве ионы Ca могут свободно состоянии диффундироваться в различных частях цитоплазмы, в то же время значительное количество Ca в связанном виде накапливается в различных внутриклеточных депо или в составе кальций-связывающих белков. Регуляция физиологических процессов с ионами внутриклеточного Са происходит в диапазоне концентраций 10 М, тогда как концентрация Са во внеклеточном пространстве выше и составляет 10 М, для поддержании градиента концентраций в клетках имеются важные Са транспортирующие системы плазматической мембраны, эндоплазматического ретикулума и митохондрий. В нейронах функционируют внутриклеточные ферменты и белки плазматической мембраны для поддержания Са-гомеостаза и реализации механизмов внутриклеточной сигнализации для обеспечения жизнедеятельности в выживании клеток. Нарушение или гиперактивация одного или нескольких механизмов кальциевой сигнализации может привести к повреждению и гибели нейронов в случае отсутствия компенсаторных механизмов. Ca ions are a key messenger for the regulation of most of the physiological functions of cells. Inside the cell, Ca ions can freely diffuse in various parts of the cytoplasm, but a significant amount of Ca is also bound in various intracellular depots or in the form of calcium-binding proteins. The regulation of physiological processes by intracellular Ca ions occurs in the concentration range of 10 M, and the concentration of Ca in the extracellular space is higher and is 10 M, and to maintain this concentration gradient, cells have Ca-transporting systems of the plasma membrane, endoplasmic reticulum and mitochondria. In neurons, a large number of intracellular enzymes and plasma membrane proteins function to maintain Ca-homeostasis and implement intracellular signaling mechanisms to ensure vital activity in the survival of cells. Violation or hyperactivation of one or more mechanisms of calcium signaling can lead to cell damage and death in the absence of compensatory mechanisms.

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Wang, Shi Qiang, Edward G. Lakatta, Heping Cheng, and Zeng Quan Zhou. "Adaptive mechanisms of intracellular calcium homeostasis in mammalian hibernators." Journal of Experimental Biology 205, no. 19 (October 1, 2002): 2957–62. http://dx.doi.org/10.1242/jeb.205.19.2957.

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SUMMARYIntracellular Ca2+ homeostasis is a prerequisite for a healthy cell life. While cells from some mammals may suffer dysregulation of intracellular Ca2+ levels under certain deleterious and stressful conditions, including hypothermia and ischemia, cells from mammalian hibernators exhibit a remarkable ability to maintain a homeostatic intracellular Ca2+ environment. Compared with cells from non-hibernators, hibernator cells are characterized by downregulation of the activity of Ca2+ channels in the cell membrane, which helps to prevent excessive Ca2+ entry. Concomitantly, sequestration of Ca2+ by intracellular Ca2+ stores, especially the sarcoplasmic/endoplasmic reticulum, is enhanced to keep the resting levels of intracellular Ca2+ stable. An increase in stored Ca2+ in heart cells during hibernation ensures that the levels of Ca2+messenger are sufficient for forceful cell contraction under conditions of hypothermia. Maintenance of Na+ gradients, viaNa+—Ca2+ exchangers, is also important in the Ca2+ homeostasis of hibernator cells. Understanding the adaptive mechanisms of Ca2+ regulation in hibernating mammals may suggest new strategies to protect nonhibernator cells, including those of humans, from Ca2+-induced dysfunction.

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Li, Li, Hao-Jan Tsai, Lin Li, and Xue-Mei Wang. "Icariin Inhibits the Increased Inward Calcium Currents Induced by Amyloid-β25-35 Peptide in CA1 Pyramidal Neurons of Neonatal Rat Hippocampal Slice." American Journal of Chinese Medicine 38, no. 01 (January 2010): 113–25. http://dx.doi.org/10.1142/s0192415x10007701.

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Overload of intracellular calcium caused by amyloid-β peptide has been implicated in the pathogenesis of neuronal damage in Alzheimer's disease. Voltage-gated calcium channels (VGCCs) provide one of the major sources of Ca2+ entry into cells. Here, we investigated whether icariin had effect on the changes of calcium currents induced by Aβ25-35 in hippocampal pyramidal neurons. Using whole-cell patch-clamp, we showed that Aβ25-35 enhanced the inward Ba2+ and Ca2+ currents. The currents were partially inhibited by Ni2+ and completely suppressed by Cd2+ , indicating that Aβ25-35 disrupts intracellular calcium homeostasis via the modulation of both L- and T-type channels. Furthermore, icariin nearly complete suppressed the abnormal inward calcium currents induced by Aβ25-35 in a dose-dependant manner. Our findings suggest that the potential neuroprotective effect of icariin on Aβ25-35-induced neurotoxicity via the balance intracelluar calcium homeostasis.

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Zavodnik, I. B. "Mitochondria, calcium homeostasis and calcium signaling." Biomeditsinskaya Khimiya 62, no. 3 (2016): 311–17. http://dx.doi.org/10.18097/pbmc20166203311.

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Са2+ is a very important and versatile intracellular signal which controls numerous biochemical and physiological (pathophysiological) processes in the cell. Good evidence exists that mitochondria are sensors, decoders and regulators of calcium signaling. Precise regulation of calcium signaling in the cell involves numerous molecular targets, which induce and decode changes of Са2+ concentrations in the cell (pumps, channels, Са2+-binding proteins, Са2+-dependent enzymes, localized in the cytoplasm and organelles). Mitochondrial Са2+ uniporter accumulates excess of Са2+ in mitochondria, while Na+/Са2+- and H+/Са2+-antiporters extrude Са2+ in the cytoplasm. Mitochondrial Са2+ overloading results in formation of mitochondria permeability transition pores which play an important role in cell death under many pathological conditions. Mitochondria regulate Са2+ homeostasis and control important cellular functions such as metabolism, proliferation, survival. Identification of cellular and mitochondrial Ca2+ transporters and understanding their functional mechanisms open up new prospects for their using as therapeutic targets

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Magi, Simona, Pasqualina Castaldo, Maria Loredana Macrì, Marta Maiolino, Alessandra Matteucci, Guendalina Bastioli, Santo Gratteri, Salvatore Amoroso, and Vincenzo Lariccia. "Intracellular Calcium Dysregulation: Implications for Alzheimer’s Disease." BioMed Research International 2016 (2016): 1–14. http://dx.doi.org/10.1155/2016/6701324.

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Alzheimer’s Disease (AD) is a neurodegenerative disorder characterized by progressive neuronal loss. AD is associated with aberrant processing of the amyloid precursor protein, which leads to the deposition of amyloid-βplaques within the brain. Together with plaques deposition, the hyperphosphorylation of the microtubules associated protein tau and the formation of intraneuronal neurofibrillary tangles are a typical neuropathological feature in AD brains. Cellular dysfunctions involving specific subcellular compartments, such as mitochondria and endoplasmic reticulum (ER), are emerging as crucial players in the pathogenesis of AD, as well as increased oxidative stress and dysregulation of calcium homeostasis. Specifically, dysregulation of intracellular calcium homeostasis has been suggested as a common proximal cause of neural dysfunction in AD. Aberrant calcium signaling has been considered a phenomenon mainly related to the dysfunction of intracellular calcium stores, which can occur in both neuronal and nonneuronal cells. This review reports the most recent findings on cellular mechanisms involved in the pathogenesis of AD, with main focus on the control of calcium homeostasis at both cytosolic and mitochondrial level.

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Steendijk, Paul. "Sepsis and intracellular calcium homeostasis, a sparkling story*." Critical Care Medicine 33, no. 3 (March 2005): 688–90. http://dx.doi.org/10.1097/01.ccm.0000155773.51773.44.

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Todd, James C., and Daniel L. Mollitt. "Effect of sepsis on erythrocyte intracellular calcium homeostasis." Critical Care Medicine 23, no. 3 (March 1995): 459–65. http://dx.doi.org/10.1097/00003246-199503000-00008.

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Engedal, Nikolai, Maria L. Torgersen, Ingrid J. Guldvik, Stefan J. Barfeld, Daniela Bakula, Frank Sætre, Linda K. Hagen, et al. "Modulation of intracellular calcium homeostasis blocks autophagosome formation." Autophagy 9, no. 10 (October 25, 2013): 1475–90. http://dx.doi.org/10.4161/auto.25900.

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Costas-Ferreira, Carmen, and Lilian R. F. Faro. "Systematic Review of Calcium Channels and Intracellular Calcium Signaling: Relevance to Pesticide Neurotoxicity." International Journal of Molecular Sciences 22, no. 24 (December 13, 2021): 13376. http://dx.doi.org/10.3390/ijms222413376.

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Pesticides of different chemical classes exert their toxic effects on the nervous system by acting on the different regulatory mechanisms of calcium (Ca2+) homeostasis. Pesticides have been shown to alter Ca2+ homeostasis, mainly by increasing its intracellular concentration above physiological levels. The pesticide-induced Ca2+ overload occurs through two main mechanisms: the entry of Ca2+ from the extracellular medium through the different types of Ca2+ channels present in the plasma membrane or its release into the cytoplasm from intracellular stocks, mainly from the endoplasmic reticulum. It has also been observed that intracellular increases in the Ca2+ concentrations are maintained over time, because pesticides inhibit the enzymes involved in reducing its levels. Thus, the alteration of Ca2+ levels can lead to the activation of various signaling pathways that generate oxidative stress, neuroinflammation and, finally, neuronal death. In this review, we also discuss some proposed strategies to counteract the detrimental effects of pesticides on Ca2+ homeostasis.

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Bielefeldt, K., C. A. Whiteis, R. V. Sharma, F. M. Abboud, and J. L. Conklin. "Reactive oxygen species and calcium homeostasis in cultured human intestinal smooth muscle cells." American Journal of Physiology-Gastrointestinal and Liver Physiology 272, no. 6 (June 1, 1997): G1439—G1450. http://dx.doi.org/10.1152/ajpgi.1997.272.6.g1439.

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Reactive oxygen species (ROS) significantly alter cell function. We examined the effects of hydrogen peroxide (H2O2) and xanthine/xanthine oxidase (X/XO) on isolated intestinal muscle cells. We assessed cell viability with the exclusion dye trypan blue and assayed the effects of H2O2 and X/XO on the intracellular redox state with the fluorescent probe 2',7'-dichlorofluorescein. Intracellular calcium concentration was measured in cells loaded with fura 2-acetoxymethyl ester, and we recorded whole membrane currents with conventional patch-clamp methods. Cells remained viable after a 5-min exposure to H2O2 and X/XO. H2O2 and X/XO led to a significant rise of the intracellular concentration of ROS. H2O2 (270 microM to 2.7 mM) as well as X/XO (0.25-16 mU; 0.5 mM xanthine) significantly increased intracellular calcium concentrations. Depletion of intracellular calcium with ryanodine or thapsigargin did not abolish the effect of ROS on the intracellular calcium concentration. In the absence of external calcium or in the presence of the calcium channel blocker nifedipine, H2O2 and X/XO still increased the intracellular calcium level. Thus calcium influx and calcium release from internal stores contributed to this rise in cytosolic calcium. Catalase and superoxide dismutase blunted or completely abolished the changes in calcium concentration elicited by H2O2 and X/XO. Exposure to ROS resulted in a rapid decline of the membrane resistance without significant changes in voltage-sensitive ion currents. We conclude that ROS disrupt the calcium homeostasis of cells at concentrations that do not lead to immediate cell death. The resulting elevation in cytosolic free calcium will activate a variety of biochemical reactions and may thus contribute to the cytotoxicity of reactive oxygen molecules.

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Nelson, K. M., and J. A. Spitzer. "Alteration of adipocyte calcium homeostasis by Escherichia coli endotoxin." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 248, no. 3 (March 1, 1985): R331—R338. http://dx.doi.org/10.1152/ajpregu.1985.248.3.r331.

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The present study evaluated calcium homeostasis in rat adipocytes after either in vivo or in vitro exposure to Escherichia coli endotoxin. Fat cells from endotoxin-treated rats showed an enhanced uptake of 45Ca. In an attempt to differentiate between 45Ca binding to the cell surface and intracellular 45Ca accumulation, adipocytes were exposed to 5 mM LaCl3. The amount of 45Ca remaining associated with lanthanum-treated adipocytes was taken to be located intracellularly and was increased in adipocytes from endotoxin-treated rats. The amount of 45Ca displaced by lanthanum was also increased in adipocytes from endotoxin-treated rats. This suggested that the endotoxin-induced increase of 45Ca accumulation included both cell surface and intracellular binding sites. Compartmental analysis of the exchange kinetics of cell-associated 45Ca with 40Ca in the medium indicated a 77% increase in the size of the cell surface compartment of adipocytes from endotoxin-treated rats compared with controls. In addition, endotoxin treatment altered the flux of calcium from the cells to the medium. In vitro exposure of freshly prepared adipocytes to 250 or 750 micrograms endotoxin/ml did not produce a perturbation of adipocyte calcium homeostasis. The results indicate that endotoxin induces alterations in the ability of adipocytes to regulate calcium translocations, suggesting that some metabolic and hormonal aspects of endotoxins' actions may be mediated through perturbation of cellular calcium homeostasis.

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Chen, Xingjuan, Ruiyuan Cao, and Wu Zhong. "Host Calcium Channels and Pumps in Viral Infections." Cells 9, no. 1 (December 30, 2019): 94. http://dx.doi.org/10.3390/cells9010094.

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Ca2+ is essential for virus entry, viral gene replication, virion maturation, and release. The alteration of host cells Ca2+ homeostasis is one of the strategies that viruses use to modulate host cells signal transduction mechanisms in their favor. Host calcium-permeable channels and pumps (including voltage-gated calcium channels, store-operated channels, receptor-operated channels, transient receptor potential ion channels, and Ca2+-ATPase) mediate Ca2+ across the plasma membrane or subcellular organelles, modulating intracellular free Ca2+. Therefore, these Ca2+ channels or pumps present important aspects of viral pathogenesis and virus–host interaction. It has been reported that viruses hijack host calcium channels or pumps, disturbing the cellular homeostatic balance of Ca2+. Such a disturbance benefits virus lifecycles while inducing host cells’ morbidity. Evidence has emerged that pharmacologically targeting the calcium channel or calcium release from the endoplasmic reticulum (ER) can obstruct virus lifecycles. Impeding virus-induced abnormal intracellular Ca2+ homeostasis is becoming a useful strategy in the development of potent antiviral drugs. In this present review, the recent identified cellular calcium channels and pumps as targets for virus attack are emphasized.

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Li, Guohui, Wenxuan Fu, Yu Deng, and Yunying Zhao. "Role of Calcium/Calcineurin Signalling in Regulating Intracellular Reactive Oxygen Species Homeostasis in Saccharomyces cerevisiae." Genes 12, no. 9 (August 25, 2021): 1311. http://dx.doi.org/10.3390/genes12091311.

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The calcium/calcineurin signalling pathway is required for cell survival under various environmental stresses. Using Saccharomyces cerevisiae, we explored the mechanism underlying calcium-regulated homeostasis of intracellular reactive oxygen species (ROS). We found that deletion of acyltransferase Akr1 and C-5 sterol desaturase Erg3 increased the intracellular ROS levels and cell death, and this could be inhibited by the addition of calcium. The hexose transporter Hxt1 and the amino acid permease Agp1 play crucial roles in maintaining intracellular ROS levels, and calcium induced the expression of the HXT1 and AGP1 genes. The cytosolic calcium concentration was decreased in both the akr1Δ and erg3Δ mutants relative to wild-type cells, potentially lowering basal expression of HXT1 and AGP1. Moreover, the calcium/calcineurin signalling pathway also induced the expression of AKR1 and ERG3, indicating that Akr1 and Erg3 might perform functions that help yeast cells to survive under high calcium concentrations. Our results provided mechanistic insight into how calcium regulated intracellular ROS levels in yeast.

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BRUNE, Bernhard, and Volker ULLRICH. "Cyclic nucleotides and intracellular-calcium homeostasis in human platelets." European Journal of Biochemistry 207, no. 2 (July 1992): 607–13. http://dx.doi.org/10.1111/j.1432-1033.1992.tb17087.x.

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SZIKRA, TAMAS, and DAVID KRIŽAJ. "Intracellular organelles and calcium homeostasis in rods and cones." Visual Neuroscience 24, no. 5 (September 2007): 733–43. http://dx.doi.org/10.1017/s0952523807070587.

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The role of intracellular organelles in Ca2+homeostasis was studied in salamander rod and cone photoreceptors under conditions that simulate photoreceptor activation by darkness and light. Sustained depolarization evoked a Ca2+gradient between the cell body and ellipsoid regions of the inner segment (IS). The standing pattern of calcium fluxes was created by interactions between the plasma membrane, endoplasmic reticulum (ER), and mitochondria. Pharmacological experiments suggested that mitochondria modulate both baseline [Ca2+]i in hyperpolarized cells as well as kinetics of Ca2+entry via L type Ca2+channels in cell bodies and ellipsoids of depolarized rods and cones. Inhibition of mitochondrial Ca2+sequestration by antimycin/oligomycin caused a three-fold reduction in the amount of Ca2+accumulated into intracellular organelles in both cell bodies and ellipsoids. A further 50% decrease in intracellular Ca2+content within cell bodies, but not ellipsoids, was observed after suppression of SERCA-mediated Ca2+uptake into the ER. Inhibition of Ca2+sequestration into the endoplasmic reticulum by thapsigargin or cyclopiazonic acid decreased the magnitude and kinetics of depolarization-evoked Ca2+signals in cell bodies of rods and cones and decreased the amount of Ca2+accumulated into internal stores. These results suggest that steady-state [Ca2+]i in photoreceptors is regulated in a region-specific manner, with the ER contribution predominant in the cell body and mitochondrial buffering [Ca2+] the ellipsoid. Local [Ca2+]i levels are set by interactions between the plasma membrane Ca2+channels and transporters, ER and mitochondria. Mitochondria are likely to play an essential role in temporal and spatial buffering of photoreceptor Ca2+.

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Piccolini, Valeria Maria, Maria Grazia Bottone, Giovanni Bottiroli, Sandra Angelica De Pascali, Francesco Paolo Fanizzi, and Graziella Bernocchi. "Platinum drugs and neurotoxicity: effects on intracellular calcium homeostasis." Cell Biology and Toxicology 29, no. 5 (August 28, 2013): 339–53. http://dx.doi.org/10.1007/s10565-013-9252-3.

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Sato, Hideomi, Junji Hori, Munetaka Saito, Yoshiaki Habara, and Koichi Kawahara. "Glutamate-induced neurotoxicity and intracellular calcium homeostasis in neurons." Neuroscience Research 31 (January 1998): S136. http://dx.doi.org/10.1016/s0168-0102(98)82034-8.

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Bagur Quetglas, Rafaela, Péter Várnai, Gyorgy Csordás, and Gyorgy Hajnóczky. "Effect of Arsenic on Intracellular Calcium & Redox Homeostasis." Biophysical Journal 112, no. 3 (February 2017): 132a. http://dx.doi.org/10.1016/j.bpj.2016.11.730.

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Florea, A. M., and D. Büsselberg. "Toxic effects of metals: modulation of intracellular calcium homeostasis." Materialwissenschaft und Werkstofftechnik 36, no. 12 (December 2005): 757–60. http://dx.doi.org/10.1002/mawe.200500960.

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Bkaily, Ghassan, and Danielle Jacques. "Calcium Homeostasis, Transporters, and Blockers in Health and Diseases of the Cardiovascular System." International Journal of Molecular Sciences 24, no. 10 (May 15, 2023): 8803. http://dx.doi.org/10.3390/ijms24108803.

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Calcium is a highly positively charged ionic species. It regulates all cell types’ functions and is an important second messenger that controls and triggers several mechanisms, including membrane stabilization, permeability, contraction, secretion, mitosis, intercellular communications, and in the activation of kinases and gene expression. Therefore, controlling calcium transport and its intracellular homeostasis in physiology leads to the healthy functioning of the biological system. However, abnormal extracellular and intracellular calcium homeostasis leads to cardiovascular, skeletal, immune, secretory diseases, and cancer. Therefore, the pharmacological control of calcium influx directly via calcium channels and exchangers and its outflow via calcium pumps and uptake by the ER/SR are crucial in treating calcium transport remodeling in pathology. Here, we mainly focused on selective calcium transporters and blockers in the cardiovascular system.

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Mailhot, Geneviève, Jean-Luc Petit, Christian Demers, and Marielle Gascon-Barré. "Influence of the in Vivo Calcium Status on Cellular Calcium Homeostasis and the Level of the Calcium-Binding Protein Calreticulin in Rat Hepatocytes*." Endocrinology 141, no. 3 (March 1, 2000): 891–900. http://dx.doi.org/10.1210/endo.141.3.7398.

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Abstract Little attention has been given to the consequences of the in vivo calcium status on intracellular calcium homeostasis despite several pathological states induced by perturbations of the in vivo calcium balance. The aim of these studies was to probe the influence of an in vivo calcium deficiency on the resting cytoplasmic Ca2+ concentration and the inositol-1,4,5-trisphosphate-sensitive Ca2+ pools. Studies were conducted in hepatocytes (a cell type well characterized for its cellular Ca2+ response) isolated from normal and calcium-deficient rats secondary to vitamin D depletion. Both resting cytoplasmic Ca2+ concentration and Ca2+ mobilization from inositol-1,4,5-trisphosphate -sensitive cellular pools were significantly lowered by calcium depletion. In addition, Ca deficiency was shown to significantly reduce calreticulin messenger RNA and protein levels but calcium entry through store-operated calcium channels remained unaffected, indicating that the Ca2+ entry mechanisms are still fully operational in calcium deficiency. The effects of calcium deficiency on cellular calcium homeostasis were reversible by repletion with oral calcium feeding alone or by the administration of the calcium-regulating hormone 1,25-dihydroxyvitamin D3, further strengthening the tight link between extra- and intracellular calcium. These data, therefore, challenge the currently prevailing hypothesis that extracellular Ca2+ has no significant impact on cellular Ca2+ by demonstrating that despite the large Ca2+ gradient between extra- and intracellular Ca2+ concentrations, calcium deficiency in vivo significantly alters the hormone-sensitive cellular calcium homeostasis.

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Verma, Chaitenya, Ankush Kumar Rana, Vandana Anang, Brijendra K. Tiwari, Aayushi Singh, Shakuntala Surender Kumar Saraswati, Malini Shariff, and Krishnamurthy Natarajan. "Calcium Dynamics Regulate Protective Responses and Growth of Staphylococcus aureus in Macrophages." Biomolecular Concepts 11, no. 1 (January 1, 2020): 230–39. http://dx.doi.org/10.1515/bmc-2020-0021.

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Abstract Staphylococcus aureus (S. aureus) is a gram-positive bacteria, which causes various fatal respiratory infections including pneumonia. The emergence of Methicillin-Resistance Staphylococcus aureus (MRSA) demands a thorough understanding of host-pathogen interactions. Here we report the role of calcium in regulating defence responses of S. aureus in macrophages. Regulating calcium fluxes in cells by different routes differentially governs the expression of T cell costimulatory molecule CD80 and Th1 promoting IL-12 receptor. Inhibiting calcium influx from extracellular medium increased expression of IFN-γ and IL-10 while blocking calcium release from the intracellular stores inhibited TGF-β levels. Blocking voltage-gated calcium channels (VGCC) inhibited the expression of multiple cytokines. While VGCC regulated the expression of apoptosis protein Bax, extracellular calcium-regulated the expression of Cytochrome-C. Similarly, VGCC regulated the expression of autophagy initiator Beclin-1. Blocking VGCC or calcium release from intracellular stores promoted phagosome-lysosome fusion, while activating VGCC inhibited phagosomelysosome fusion. Finally, calcium homeostasis regulated intracellular growth of Staphylococcus, although using different mechanisms. While blocking extracellular calcium influx seems to rely on IFN-γ and IL-12Rβ receptor mediated reduction in bacterial survival, blocking either intracellular calcium release or via VGCC route seem to rely on enhanced autophagy mediated reduction of intracellular bacterial survival. These results point to fine-tuning of defence responses by routes of calcium homeostasis.

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Zhu, L., G. A. Herrera, C. R. White, and P. W. Sanders. "Immunoglobulin light chain alters mesangial cell calcium homeostasis." American Journal of Physiology-Renal Physiology 272, no. 3 (March 1, 1997): F319—F324. http://dx.doi.org/10.1152/ajprenal.1997.272.3.f319.

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This study examined the hypothesis that certain immunoglobulin light chains directly altered mesangial cell calcium homeostasis. Intracellular Ca2+ concentration (intracellular [Ca2+]) signaling was determined in suspensions of rat mesangial cells using the acetoxymethyl ester of fura 2 with a calcium removal/replacement protocol. Pretreatment of cultured rat mesangial cells with a glomerulopathic kappa-light chain (gle) produced reversible dose- and time-dependent attenuation of ATP- and thrombin-evoked [Ca2+] transients (189 +/- 24 vs. 126 +/- 10 nM, P < 0.05 with ATP; 198 +/- 5 vs. 117 +/- 3 nM, P < 0.05 with thrombin) and capacitative calcium influx (199 +/- 14 vs. 142 +/- 17 nM, P < 0.05 for ATP; 252 +/- 19 vs. 198 +/- 18 nM, P < 0.05 for thrombin). Mesangial cells treated with gle and supplemented with myo-inositol (450 microM) did not demonstrate the attenuation of the ATP-evoked [Ca2+] transient and capacitative calcium influx. Gle also decreased mean [Ca2+] transient (80 +/- 7 vs. 56 +/- 1 nM, P < 0.05) and capacitative calcium influx (306 +/- 10 vs. 241 +/- 4 nM, P < 0.05) in response to thapsigargin, a Ca2+-adenosinetriphosphatase inhibitor. This inhibition was not reversed by exogenous myo-inositol. Another kappa-light chain (10 microg/ml) did not affect mesangial cell calcium signaling. Deranged mesangial cell calcium homeostasis by certain light chains may play a central pathogenetic role in glomerulosclerosis associated with deposition of immunoglobulin light chains.

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Mohr, F. C., and C. Fewtrell. "The effect of mitochondrial inhibitors on calcium homeostasis in tumor mast cells." American Journal of Physiology-Cell Physiology 258, no. 2 (February 1, 1990): C217—C226. http://dx.doi.org/10.1152/ajpcell.1990.258.2.c217.

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The depletion of intracellular ATP by mitochondrial inhibitors in a glucose-free saline solution inhibited antigen-stimulated 45Ca uptake, the rise in cytoplasmic calcium, measured by fura-2, and secretion in rat basophilic leukemia cells. Lowering the intracellular ATP concentration also released calcium from an intracellular store and made further 45Ca efflux from the cells unresponsive to subsequent antigen stimulation. Antigen-stimulated 45Ca efflux could be restored by the addition of glucose. The ATP-sensitive calcium store appeared to be the same store that releases calcium in response to antigen. In contrast, intracellular ATP was not lowered, and antigen-stimulated secretion was unaffected by mitochondrial inhibitors, provided that glucose was present in the bathing solution. Similarly, antigen-stimulated 45Ca uptake, 45Ca efflux, and the rise in free ionized calcium were unaffected by individual mitochondrial inhibitors in the presence of glucose. However, when the respiratory chain inhibitor antimycin A was used in combination with the ATP synthetase inhibitor oligomycin in the presence of glucose, antigen-stimulated 45Ca uptake was inhibited, whereas the rise in free ionized calcium and secretion were unaffected. Also, antigen-induced depolarization (an indirect measurement of Ca2+ influx across the plasma membrane) was not affected. The inhibition of antigen-stimulated 45Ca uptake could, however, be overcome if a high concentration of the Ca2+ buffer quin2 was present in the cells to buffer the incoming 45Ca. These results suggest that in fully functional rat basophilic leukemia cells the majority of the calcium entering in response to antigen stimulation is initially buffered by a calcium store sensitive to antimycin A and oligomycin, presumably the mitochondria.

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Deshpande, Laxmikant S., Robert J. DeLorenzo, Severn B. Churn, and J. Travis Parsons. "Neuronal-Specific Inhibition of Endoplasmic Reticulum Mg2+/Ca2+ ATPase Ca2+ Uptake in a Mixed Primary Hippocampal Culture Model of Status Epilepticus." Brain Sciences 10, no. 7 (July 10, 2020): 438. http://dx.doi.org/10.3390/brainsci10070438.

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Loss of intracellular calcium homeostasis is an established mechanism associated with neuronal dysfunction and status epilepticus. Sequestration of free cytosolic calcium into endoplasmic reticulum by Mg2+/Ca2+ adenosinetriphosphatase (ATPase) is critical for maintenance of intracellular calcium homeostasis. Exposing hippocampal cultures to low-magnesium media is a well-accepted in vitro model of status epilepticus. Using this model, it was shown that endoplasmic reticulum Ca2+ uptake was significantly inhibited in homogenates from cultures demonstrating electrophysiological seizure phenotypes. Calcium uptake was mainly neuronal. However, glial Ca2+ uptake was also significantly inhibited. Viability of neurons exposed to low magnesium was similar to neurons exposed to control solutions. Finally, it was demonstrated that Ca2+ uptake inhibition and intracellular free Ca2+ levels increased in parallel with increasing incubation in low magnesium. The results suggest that inhibition of Mg2+/Ca2+ ATPase-mediated endoplasmic reticulum Ca2+ sequestration contributes to loss of intracellular Ca2+ homeostasis associated with status epilepticus. This study describes for the first time inhibition of endoplasmic reticulum Mg2+/Ca2+ ATPase in a mixed primary hippocampal model of status epilepticus. In combination with animal models of status epilepticus, the cell culture model provides a powerful tool to further elucidate mechanisms that result in inhibition of Mg2+/Ca2+ ATPase and downstream consequences of decreased enzyme activity.

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Križaj, David, Aaron J. Mercer, Wallace B. Thoreson, and Peter Barabas. "Intracellular pH modulates inner segment calcium homeostasis in vertebrate photoreceptors." American Journal of Physiology-Cell Physiology 300, no. 1 (January 2011): C187—C197. http://dx.doi.org/10.1152/ajpcell.00264.2010.

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Neuronal metabolic and electrical activity is associated with shifts in intracellular pH (pHi) proton activity and state-dependent changes in activation of signaling pathways in the plasma membrane, cytosol, and intracellular compartments. We investigated interactions between two intracellular messenger ions, protons and calcium (Ca2+), in salamander photoreceptor inner segments loaded with Ca2+ and pH indicator dyes. Resting cytosolic pH in rods and cones in HEPES-based saline was acidified by ∼0.4 pH units with respect to pH of the superfusing saline (pH = 7.6), indicating that dissociated inner segments experience continuous acid loading. Cytosolic alkalinization with ammonium chloride (NH4Cl) depolarized photoreceptors and stimulated Ca2+ release from internal stores, yet paradoxically also evoked dose-dependent, reversible decreases in [Ca2+]i. Alkalinization-evoked [Ca2+]i decreases were independent of voltage-operated and store-operated Ca2+ entry, plasma membrane Ca2+ extrusion, and Ca2+ sequestration into internal stores. The [Ca2+]i-suppressive effects of alkalinization were antagonized by the fast Ca2+ buffer BAPTA, suggesting that pHi directly regulates Ca2+ binding to internal anionic sites. In summary, this data suggest that endogenously produced protons continually modulate the membrane potential, release from Ca2+ stores, and intracellular Ca2+ buffering in rod and cone inner segments.

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Winston, F. K., L. E. Thibault, and E. J. Macarak. "An Analysis of the Time-Dependent Changes in Intracellular Calcium Concentration in Endothelial Cells in Culture Induced by Mechanical Stimulation." Journal of Biomechanical Engineering 115, no. 2 (May 1, 1993): 160–68. http://dx.doi.org/10.1115/1.2894116.

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When bovine pulmonary artery endothelial cells in culture are subjected to mechanical strain, their physiology is altered. Experimentally, this mechanical strain is generated by increased tension in the substrate to which the cells are attached and results in altered levels of fibronectin. Studies of the structural response of the endothelial cell suggest that this stimulus is transmitted to the cell membrane, organelles, and cytoskeleton by natural cell attachments in a quantifiable and predictable manner. This report examines altered intracellular calcium homeostasis as a possible messenger for the observed strain-induced physiologic response. In particular, using the intracellularly trapped calcium indicator dyes, Quin2 and Fura2, we observed changes in cytosolic free calcium ion concentration in response to biaxial strain of bovine pulmonary artery endothelial cells in culture. The magnitude and time course of this calcium transient resemble that produced by treatment with the calcium ionophore, Ionomycin, indicating that mechanical stimulation may alter cell membrane permeability to calcium. Additional experiments in the presence of EDTA indicated that calcium was also released from intracellular stores in response to strain. In order to explain the stretch-induced calcium transients, a first-order species conservation model is presented that takes into account both the cell’s structural response and the calcium homeostatic mechanisms of the cell. It is hypothesized that the cell’s calcium sequestering and pumping capabilities balanced with its mechanically induced changes in calcium ion permeability will determine the level and time course of calcium accumulation in the cytosol.

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Liao, Jing, Wenju Lu, Yuqin Chen, Xin Duan, Chenting Zhang, Xiaoyun Luo, Ziying Lin, et al. "Upregulation of Piezo1 (Piezo Type Mechanosensitive Ion Channel Component 1) Enhances the Intracellular Free Calcium in Pulmonary Arterial Smooth Muscle Cells From Idiopathic Pulmonary Arterial Hypertension Patients." Hypertension 77, no. 6 (June 2021): 1974–89. http://dx.doi.org/10.1161/hypertensionaha.120.16629.

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Emerging studies have reported the mechanosensitive Piezo1 (piezo type mechanosensitive ion channel component 1) plays essential roles in regulating the vascular tone through mechanistic actions on intracellular calcium homeostasis. However, the specific roles of Piezo1 in pulmonary vessels remain incompletely understood. We aim to investigate whether and how Piezo1 regulates the intracellular calcium homeostasis in human pulmonary arterial smooth muscle cells (PASMCs) under normal and pulmonary arterial hypertension (PAH) conditions. Cultured human PASMCs isolated from both control donors and idiopathic PAH patients were used as cell models. Fura-2 based intracellular calcium imaging was performed to measure the intracellular free calcium concentration ([Ca 2+ ] i ). Results showed that activation of Piezo1 by Yoda1 increases [Ca 2+ ] i by inducing both intracellular calcium release from internal calcium stores through the intracellular (intra-) Piezo1 localized at the subcellular organelles, including endoplasmic reticulum/sarcoplasmic reticulum, mitochondria, and nucleus; as well as extracellular calcium influx through the plasma membrane-localized Piezo1 in a mechanism independent of the store-operated calcium entry. Moreover, the Piezo1-mediated increase of [Ca 2+ ] i is linked to increased contraction and proliferation of PASMCs. Yoda1 induces dose-dependent vasocontraction in endothelium-denuded rat intrapulmonary arteries. Significant upregulation and increased activity of Piezo1 were observed in idiopathic PAH-PASMCs versus donor-PASMCs, contributing to the increased [Ca 2+ ] i and excessive proliferation of idiopathic PAH-PASMCs. In summary, Piezo1 mediates the increase of [Ca 2+ ] i by triggering both intracellular calcium release and extracellular influx. The enhanced Piezo1 expression and activity accounts, at least partially, for the abnormally elevated [Ca 2+ ] i and proliferation in idiopathic PAH-PASMCs.

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Villalba, M., A. Martínez-Serrano, P. Gómez-Puertas, P. Blanco, C. Börner, A. Villa, M. Casado, C. Giménez, R. Pereira, and E. Bogonez. "The role of pyruvate in neuronal calcium homeostasis. Effects on intracellular calcium pools." Journal of Biological Chemistry 269, no. 4 (January 1994): 2468–76. http://dx.doi.org/10.1016/s0021-9258(17)41969-7.

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Deshpande, Deepak A., Thomas A. White, Soner Dogan, Timothy F. Walseth, Reynold A. Panettieri, and Mathur S. Kannan. "CD38/cyclic ADP-ribose signaling: role in the regulation of calcium homeostasis in airway smooth muscle." American Journal of Physiology-Lung Cellular and Molecular Physiology 288, no. 5 (May 2005): L773—L788. http://dx.doi.org/10.1152/ajplung.00217.2004.

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The contractility of airway smooth muscle cells is dependent on dynamic changes in the concentration of intracellular calcium. Signaling molecules such as inositol 1,4,5-trisphosphate and cyclic ADP-ribose play pivotal roles in the control of intracellular calcium concentration. Alterations in the processes involved in the regulation of intracellular calcium concentration contribute to the pathogenesis of airway diseases such as asthma. Recent studies have identified cyclic ADP-ribose as a calcium-mobilizing second messenger in airway smooth muscle cells, and modulation of the pathway involved in its metabolism results in altered calcium homeostasis and may contribute to airway hyperresponsiveness. In this review, we describe the basic mechanisms underlying the dynamics of calcium regulation and the role of CD38/cADPR, a novel pathway, in the context of airway smooth muscle function and its contribution to airway diseases such as asthma.

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Hamilton, Shanna, and Dmitry Terentyev. "Altered Intracellular Calcium Homeostasis and Arrhythmogenesis in the Aged Heart." International Journal of Molecular Sciences 20, no. 10 (May 14, 2019): 2386. http://dx.doi.org/10.3390/ijms20102386.

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Aging of the heart is associated with a blunted response to sympathetic stimulation, reduced contractility, and increased propensity for arrhythmias, with the risk of sudden cardiac death significantly increased in the elderly population. The altered cardiac structural and functional phenotype, as well as age-associated prevalent comorbidities including hypertension and atherosclerosis, predispose the heart to atrial fibrillation, heart failure, and ventricular tachyarrhythmias. At the cellular level, perturbations in mitochondrial function, excitation-contraction coupling, and calcium homeostasis contribute to this electrical and contractile dysfunction. Major determinants of cardiac contractility are the intracellular release of Ca2+ from the sarcoplasmic reticulum by the ryanodine receptors (RyR2), and the following sequestration of Ca2+ by the sarco/endoplasmic Ca2+-ATPase (SERCa2a). Activity of RyR2 and SERCa2a in myocytes is not only dependent on expression levels and interacting accessory proteins, but on fine-tuned regulation via post-translational modifications. In this paper, we review how aberrant changes in intracellular Ca2+ cycling via these proteins contributes to arrhythmogenesis in the aged heart.

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Zhou, Xinyu, Peihui Lin, Daiju Yamazaki, Ki Ho Park, Shinji Komazaki, S. R. Wayne Chen, Hiroshi Takeshima, and Jianjie Ma. "Trimeric Intracellular Cation Channels and Sarcoplasmic/Endoplasmic Reticulum Calcium Homeostasis." Circulation Research 114, no. 4 (February 14, 2014): 706–16. http://dx.doi.org/10.1161/circresaha.114.301816.

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Todd, James C., and Daniel L. Mollitt. "LEUKOCYTE MODULATION INHIBITS ENDOTOXIN-INDUCED DISRUPTION OF INTRACELLULAR CALCIUM HOMEOSTASIS." Journal of Trauma: Injury, Infection, and Critical Care 37, no. 6 (December 1994): 1018–19. http://dx.doi.org/10.1097/00005373-199412000-00058.

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Todd, James C., and Daniel L. Mollitt. "Leukocyte Modulation Inhibits Endotoxin-Induced Disruption of Intracellular Calcium Homeostasis." Journal of Trauma: Injury, Infection, and Critical Care 39, no. 6 (December 1995): 1148–52. http://dx.doi.org/10.1097/00005373-199512000-00024.

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Swann, John D., Mary W. Smith, Patricia C. Phelps, Atsuhiko Maki, Irene K. Berezesky, and Benjamin F. Trump. "Oxidative Injury Induces Influx-Dependent Changes in Intracellular Calcium Homeostasis." Toxicologic Pathology 19, no. 2 (February 1991): 128–37. http://dx.doi.org/10.1177/019262339101900207.

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Walden, A. P., K. M. Dibb, and A. W. Trafford. "Differences in intracellular calcium homeostasis between atrial and ventricular myocytes." Journal of Molecular and Cellular Cardiology 46, no. 4 (April 2009): 463–73. http://dx.doi.org/10.1016/j.yjmcc.2008.11.003.

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Zhang, Yanjie, Yuehong Wang, Ethan Read, Ming Fu, Yanxi Pei, Lingyun Wu, Rui Wang, and Guangdong Yang. "Golgi Stress Response, Hydrogen Sulfide Metabolism, and Intracellular Calcium Homeostasis." Antioxidants & Redox Signaling 32, no. 9 (March 20, 2020): 583–601. http://dx.doi.org/10.1089/ars.2019.7824.

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Metterlein, T., F. Schuster, L. Tadda, M. Hager, N. Roewer, and M. Anetseder. "Statins Alter Intracellular Calcium Homeostasis in Malignant Hyperthermia Susceptible Individuals." Cardiovascular Therapeutics 28, no. 6 (October 19, 2010): 356–60. http://dx.doi.org/10.1111/j.1755-5922.2010.00237.x.

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LIU, RENYI, WEI FAN, KARSTEN KRÜGER, YU XIAO, CHRISTIAN PILAT, MICHAEL SEIMETZ, ROBERT RINGSEIS, et al. "Exercise Affects T-Cell Function by Modifying Intracellular Calcium Homeostasis." Medicine & Science in Sports & Exercise 49, no. 1 (January 2017): 29–39. http://dx.doi.org/10.1249/mss.0000000000001080.

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Journal articles on the topic 'Intracellular calcium homeostasis'

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