Relevant bibliographies by topics / Intracellular calcium homeostasis

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  2. Dissertations / Theses
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Academic literature on the topic 'Intracellular calcium homeostasis'

Author: Grafiati
Published: 25 May 2024

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Journal articles on the topic "Intracellular calcium homeostasis"

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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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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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Dissertations / Theses on the topic "Intracellular calcium homeostasis"

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Vasilev, Filip. "New roles for actin-binding proteins and PIP2 in intracellular calcium homeostasis." Thesis, Open University, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.582807.

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Spatiotemporal increase of the intracellular Ca2+ is the most universal way to regulate the function of a eukaryotic cell. Owing to a host of actin-binding proteins and enzymes whose activities are modulated by the local concentration of Ca2+, free Ca2+ in cytosol serves as a pivotal second messenger in a variety of cell functions. The rise and fall of intracellular Ca2+ wave has been best illustrated in eggs at fertilization. However, the molecular mechanism by which intracellular Ca2+ is increased in the fertilized egg is largely unknown despite the discoveries of the distinct Ca2+-mobilizing second messengers in the past 30 years. In this thesis, I have used the starfish oocytes to study how Ca2+ signaling can be modulated by the actin cytoskeleton, which is known to be dynamically remodelled during meiotic maturation and fertilization of the egg. The principal issues of my experimental work are: (i) to establish the role of actin-binding proteins and PIP2 in the regulation of the Ca2+ signaling; (ii) to study the effect of the Ca2+ -store depletion on Ca2+ signaling and on the structure and function of the actin cytoskeleton, and (iii) to study the role of the actin-cytoskeleton in establishing the block to polyspermy. Microinjected into starfish eggs, actin-binding protein gelsolin, function- blocking antibody to depactin, and the PIP2-sequestering fusion protein that indirectly alters the actin cytoskeleton, all changed a certain aspect of Ca2+ signaling. Depletion of the Ca2+ store with ionomycin in turn drastically changed the cortical structure and the actin cytoskeleton of the eggs, eventually leading to a deleterious effect on egg activation and early development. Finally, the alteration of the actin cytoskeleton led to failure to establish a fast and slow block to polyspermy. Taken together, this study indicated that the actin cytoskeleton is an important factor that optimizes the Ca2+ response at egg activation and guides monospermic fertilization.
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Thor, Der. "The effect of estrogen on intracellular calcium homeostasis in human endothelial cells." Scholarly Commons, 2009. https://scholarlycommons.pacific.edu/uop_etds/2397.

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The effect of estrogen on the vasculature is mediated in part by influences on NO bioavailability. Nitric oxide (NO) is a potent vasodilator which is synthesized in endothelial cell by endothelial nitric oxide synthase (eNOS) catalyzed conversion of L-arginine to L-citrulline. Although estrogen has been shown to increase eNOS expression and/or activity, the mechanism of estrogen-mediated increased eNOS activity in endothelial cells remains elusive. The Ca 2+ /calmodulin complex is known to aid in eNOS activation by dissociating eNOS from the membrane bound protein, caveolin-1. We investigated the role of estrogen on the Ca 2+ homeostasis of the human endothelial cell line, EA.hy926, using thapsigargin (TG), a sarco(endo)plasmic reticulum Ca 2+ -ATPase, or ATP, a purinergic receptor agonist, to evoke increased intracellular calcium concentration ([Ca 2+ ] i ). [Ca 2+ ] i in Fura 2-AM-loaded EA.hy926 cell populations were measured by fluorescence spectrophotometry. Treatment of cells with 17 β-estradiol (E 2 , 1 μM, 24 hours) showed an increased agonist-evoked [Ca 2+ ] i increase due to both higher Ca 2+ release and Ca 2+ influx, which accompanied an increased eNOS protein expression. Both increased [Ca 2+ ] i and eNOS expression were attenuated with the nonselective estrogen receptor (ER) inhibitor, ICI 182,780. We further analyzed the role of ER in E 2 - mediated effects using ERα-knockdown cells. ERα-knockdown was achieved by transfecting the cells with ERα-specific siRNA. E 2 did not influence agonist-evoked [Ca 2+ ] i increase in the ERα-knockdown cells, indicating that the E 2 -mediated effects were ERα-dependent. In the vasculature, both the genomic and nongenomic effects of estrogen are mediated via ERα. In the current study, the effect of E 2 on agonist-evoked [Ca 2+ ] i increase was only observed in chronically treated (1 μM, 24 hours) cells and not acutely treated (1 μM, 5 minutes) cells, suggesting a genomic action of E 2 . The genomic action was verified by treating cells with E 2 in the presence of actinomycin D, a transcription inhibitor. Actinomycin D attenuated the effect of E 2 on agonist-evoked [Ca 2+ ] i increase. The present work revealed a transcription-dependent and ERα-mediated modulation of Ca 2+ homeostasis in human endothelial cells treated with estrogen for the long-term. This data suggests a novel mechanism by which estrogen-mediated NO release may occur in endothelial cells.
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Kipanyula, Maulilio. "Ca2+ homeostasis in familial Alzheimer's disease: a view from intracellular Ca2+ stores." Doctoral thesis, Università degli studi di Padova, 2011. http://hdl.handle.net/11577/3421718.

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Familial Alzheimer's disease (FAD) -linked mutations in presenilin 1 and 2 (PS1, PS2) have been causally implicated in neurodegeneration and eventually neuronal cell death by amyloid toxicity and perturbation of cellular Ca2+ homeostasis. The mechanism governing this latter phenomenon remains unclear. In the cytosol, upon stimulation, both exaggerated and reduced Ca2+ release have been reported in different cell lines and neurons expressing PS1 and PS2 mutants. Despite the contradicting data yet available, it is undisputable that FAD-linked PS mutants cause imbalances of cellular Ca2+ homeostasis. Recent independent reports have strongly suggested that the FAD-linked PS1 and PS2 mutants interact directly or indirectly with both the ER Ca2+ uptake and release machinery by modulating SERCA pump, IP3R- and RyR channel activity. In the study described here, we took advantage of two available lines of transgenic (tg) mice expressing a mutant PS2 alone or together with a mutant amyloid precursor protein (APP) - both linked to FAD - in order to investigate its effects on Ca2+ homeostasis in a physiological environment more relevant to the pathology under study. We particularly focused our attention on Ca2+ dysregulation in cortical neurons from tg mice either single homozygous for human PS2-N141I or double homozygous for human PS2-N141I and human APP swedish mutations. Ca2+ measurements were carried by the fura-2/AM technique. This study highlights the role of PS2-N141I in modulating Ca2+ homeostasis of cortical neurons. We have demonstrated that, irrespective of the presence of mutant APP, modest expression of PS2-N141I altered the Ca2+ dynamics of intracellular stores. The total Ca2+ content of intracellular stores is partially depleted, as demonstrated by reduced Ca2+ release upon ionomycin stimulation. Consequently, the tg neurons have reduced Ca2+ release in response to IP3-generating agonists. However, the PS2 mutant does not affect the protein expression levels for both SERCA pump and IP3Rs. Our results suggest that the PS2-N141I FAD mutant causes a functional defect in ER Ca2+ entry/exit pathways. We also show that both tg neurons express very low levels of the mutant protein but show Ca2+ dysregulation, similar quantitatively and qualitatively to that previously reported in cell lines upon transient over-expression of the same mutant protein. Conversely, measurements of Ca2+ release via RyRs revealed a novel and unexpected finding in PS2 mutant tg mice i.e. increased Ca2+ release in response to caffeine. In addition, RyR2 protein expression level was elevated in tg neurons. Upregulation of RyRs function and protein levels could save as an adaptation phenomenon to compensate the reduction in Ca2+ release via IP3Rs or a direct effect of mutant PS2 on RyR or a secondary effect. Furthermore, PS2-N141I causes alteration in neuronal Ca2+ excitability. The tg neurons had significantly elevated number of picrotoxin-evoked synchronous Ca2+ oscillations, which required extracellular Ca2+ influx but not Ca2+ release from intracellular stores. Interestingly, while Ca2+ dysregulation appeared to be similar qualitatively and quantitatively in both single and double tg mouse models, the total amount of brain Ab42 and Ab40 peptides (ELISA) as well as their ratios were strikingly different between the two tg lines. These results strongly suggest that in tg mice the expression of mutant APP and/or Ab levels have no primary effect on the store Ca2+ content at this early stage and provide evidence that the quite similar effects on Ca2+ dynamics observed in both tg mice are due to the mutant PS2. Finally, results presented in this work suggest that although Ca2+ dysregulation is an early event in FAD, it does not affect neuronal response and vulnerability to cytotoxic stimuli at this early stage. The second part of this study focused on the role of Ab42 oligomers in cellular Ca2+ dynamics. Synthetic Ab42 oligomers reduced Ca2+ release in response to IP3 generating agonists in wt neurons but did not affect the total Ca2+ content as monitored by ionomycin. Conversely, Ab42 oligomers increased the Ca2+ release induced by caffeine. It is likely that Ab42 oligomers exert their effect on the activation pathway from IP3 generating agonists to IP3Rs. However, the mechanisms through which Ab42 deranges intracellular Ca2+ homeostasis require further investigation. Nonetheless, it is conceivable that in addition to Ab42 oligomers, also intracellular Ca2+ stores could become likely therapeutic targets in FAD and AD in general
E stato dimostrato che mutazioni in presenilina 1 e 2 (PS1, PS2) legate alle forme familiari della malattia di Alzheimer (FAD) sono implicate nella neurodegenerazione e in ultima istanza nella morte cellulare per effetto della tossicità del peptide amiloide e della perturbazione dell'omeostasi del Ca2+ cellulare. Il meccanismo alla base di quest'ultimo fenomeno non è ancora stato chiarito. Si è visto che in linee cellulari e in neuroni esprimenti mutazioni in PS1 e PS2, il rilascio di Ca2+ nel citosol in seguito a stimolazione cellulare può essere sia aumentato che ridotto. Nonostante i dati contraddittori attualmente disponibili, è innegabile che i mutanti di PS legati a FAD provocano uno squilibrio nell'omeostasi del Ca2+ cellulare. Recentemente studi indipendenti hanno dimostrato che i mutanti FAD in PS1 o PS2 interagiscono sia con i meccanismi di rilascio che di accumulo di Ca2+ nel reticolo endoplasmatico (RE), modulando sia l'attività  della pompa SERCA che i canali di tipo IP3R e RyR. In questo studio abbiamo impiegato due linee già  disponibili di topi transgenici (tg) esprimenti una PS2 mutata, da sola o assieme alla Proteina Precursore dell'Amiloide (APP) (entrambe con mutazioni legate a FAD) al fine di investigarne gli effetti sull'omeostasi del Ca2+ in una condizione fisiologica più rilevante per la patologia oggetto dello studio. Abbiamo focalizzato in particolare la nostra attenzione sull'alterazione del Ca2+ in neuroni corticali ottenuti da topi tg omozigoti per il solo mutante PS2-N141I o doppi omozigoti per le proteine mutate PS2-N141I e APPswe. Le misure di Ca2+ sono state effettuate con la tecnica del Fura-2/AM. Questo studio mette in evidenza il ruolo della PS2-N141I nel modulare l'omeostasi del Ca2+ in neuroni corticali murini. Abbiamo dimostrato che, indipendentemente dalla presenza del mutante di APP, l'espressione della PS2-N141I, in quantità  moderata, inficia le dinamiche del Ca2+ dei depositi intracellulari. In particolare,i depositi del Ca2+ sono parzialmente svuotati, come dimostrato dal ridotto rilascio di Ca2+ in seguito a stimolazione con ionomicina. Conseguentemente i neuroni tg hanno un ridotto rilascio di Ca2+in risposta ad agonisti legati alla generazione di IP3. Occorre notare che la PS2 mutata non altera i livelli di espressione delle proteine SERCA e IP3R. I nostri risultati suggeriscono che il mutante FAD PS2-N141I causa un difetto funzionale nelle vie di entrata e di uscita del Ca2+ dal RE. Abbiamo inoltre dimostrato che i neuroni di entrambe le linee tg esprimono bassi livelli di proteina mutante ma mostrano un'alterazione del segnale Ca2+ qualitativamente e quantitativamente simile a quella precedentemente riportata per le linee cellulari sovra-esprimenti la stessa proteina. Al contrario, misure del rilascio di Ca2+ via RyR hanno rivelato un effetto inatteso, ovvero un aumentato rilascio di Ca2+ in risposta a caffeina nei neuroni tg. Inoltre, i livelli proteici di RyR2 sono aumentati nei neuroni tg. Un aumento della funzionalità  e dei livelli proteici di RyR2 potrebbero essere un fenomeno adattativo per compensare la riduzione del rilascio di Ca2+ via IP3R oppure essere un effetto diretto dei mutanti PS2 su RyR2 o ancora un effetto secondario. Infine abbiamo dimostrato che la PS2-N141I causa un'alterazione nell'eccitabilità  neuronale. I neuroni tg hanno un numero significativamente più elevato di oscillazioni di Ca2+ sincronizzate, evocate da picrotossina, che dipendono dall' ingresso di Ca2+ extracellulare e non dal rilascio di Ca2+ dai depositi. E interessante notare che, mentre l'alterazione del Ca2+ è qualitativamente e quantitativamente simile nei singoli e doppi tg, sia il livello totale di peptidi Ab42 e Ab40 nel tessuto cerebrale (misurati mediante ELISA) che il loro rapporto sono notevolmente diversi tra le due linee tg. Questi risultati suggeriscono che nei topi tg l'espressione di APP mutata o i livelli di Ab non hanno alcun effetto primario sul contenuto dei depositi di Ca2+ in questo stadio precoce, e suggeriscono che gli effetti sulle dinamiche del segnale Ca2+, così simili nelle due linee tg, siano dovuti alla PS2 mutata. Infine, i risultati qui presentati suggeriscono che nonostante l'alterazione del segnale Ca2+ sia un evento precoce nei neuroni a questo stadio, non altera la vulnerabilità  neuronale a stimoli citotossici che agiscono atrraverso i depositi del Ca2+ . La seconda parte di questo studio si è concentrata sul ruolo degli oligomeri di Ab42 sulle dinamiche del Ca2+ cellulare. Nei neuroni di topi wt, oligomeri di Ab42 sintetico riducono il rilascio di Ca2+ in risposta ad agonisti legati alla produzione di IP3, ma non riducono il contenuto totale di Ca2+ dei depositi misurato mediante applicazione di ionomicina. D'altra parte, gli oligomeri di Ab42 aumentano il rilascio di Ca2+ indotto da caffeina. E' probabile che gli oligomeri di Ab42 agiscano sulla via attivata dagli agonisti legati alla produzione di IP3 e sull' IP3R. I meccanismi attraverso cui Ab42 altera l'omeostasi intracellulare del Ca2+ richiedono tuttavia ulteriori indagini. In conclusione, oltre agli oligomeri di Ab42 anche i depositi intracellulari di Ca2+ possono diventare un importante bersaglio terapeutico per intervenire sulla patologia di Alzheimer familiare ma anche sulla forma sporadica
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Leustik, Martin [Verfasser]. "Listeriolysin O and Pneumolysin: Effects on intracellular calcium homeostasis and epithelial barrier integrity / Martin Leustik." Gießen : Universitätsbibliothek, 2013. http://d-nb.info/106499170X/34.

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Allan, Laura Elizabeth. "Investigating the effects of the Alzheimer's disease-associated amyloid β-peptide on intracellular calcium homeostasis." Thesis, University of Cambridge, 2010. https://www.repository.cam.ac.uk/handle/1810/283857.

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I investigated the effects of Aβ42 on the Ca2+ signalling capacity of human neuroblastoma SH-SY5Y cells and primary hippocampal cultures. I developed an in vitro model system of dissociated hippocampal neurons and glial cells in order to reflect as closely as possible the mature hippocampus. Extensive characterisation of the culture revealed that functional neuronal networks were established by day in vitro 11, as demonstrated by the occurrence of spontaneous oscillations in both membrane potential and intracellular Ca2+ levels. Neurons exhibited functional ionotropic and metabotropic signalling systems which, in turn, rendered them sensitive to cell death induced by excitotoxic stimuli. Samples of synthetic Aβ42 were prepared according to two published protocols. One protocol produced Aβ42 samples which exhibited highly dynamic aggregation kinetics, the other produced homogeneous Aβ42 oligomers which were stable in their conformational state for up to 24 hours. While both Aβ42 preparations impaired cell viability following 24-hour treatment, only Aβ42 oligomers elicited robust Ca2+ responses following their extracellular application to cells. Aβ42 oligomers elicited distinct but different effects on the Ca2+ signalling capacity of SH-SY5Y cells and primary hippocampal neurons, respectively. in SH-SY5Y cells, Aβ42 oligomers acted to deplete the content of the intracellular ER Ca2+ store, in part through InsP3 receptors and in part through an as yet unidentified leak pathway. In primary hippocampal neurons, the application of Aβ42 oligomers resulted in a sustained and elevated increase in intracellular Ca2+ concentrations. It is postulated that these early cellular events, although distinct, will ultimately converge on a common pathway resulting in dysregulation of Ca2+ homeostasis and cell death. Thus, the findings of this thesis support the mounting body of evidence implicating the role of Ca2+ dysregulation in mediating the neurotoxic effects of Aβ42 oligomers.
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Brusich, Douglas J. "Dual roles for an intracellular calcium-signaling pathway in regulating synaptic homeostasis and neuronal excitability." Diss., University of Iowa, 2015. https://ir.uiowa.edu/etd/1830.

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Neurons are specialized cells that communicate via electrical and chemical signaling. It is well-known that homeostatic mechanisms exist to potentiate neuronal output when activity falls. Likewise, while neurons rely on excitable states to function, these same excitable states must be kept in check for stable function. However, the identity of molecular factors and pathways regulating these pathways remain elusive. Chapter 2 of this thesis reports the findings from an RNA interference- and electrophysiology-based screen to identify factors necessary for the long-term maintenance of homeostatic synaptic potentiation. Data is reported to resolve a long-standing question as to the role of presynaptic Cav2-type channels in homeostatic synaptic potentiation at the Drosophila NMJ. It is shown that reduction in Cav2 channel expression and resultant activity is not sufficient to occlude homeostatic potentiation. Thus, the homeostatic block of a amino-acid substituted Cav2-type calcium channel (cacS) channel is presumed to be due to loss of a specific signaling or binding activity, but not due to overall diminishment in channel function. It is also reported that both Drosophila homologs of phospholipase Cβ (PLCβ) and its putative activator Gαq were found to be necessary for a scaling up of neurotransmitter release upon genetic ablation of glutamate receptors. These factors are canonically involved in the activation of intracellular calcium stores through the inositol trisphosphate receptor (IP3R) and the closely related ryanodine receptor (RyR). Likewise, the Drosophila homolog of Cysteine String Protein (Csp) is identified as important for long-term homeostatic potentiation. CSP has also been reported to be involved in regulation of intracellular calcium. PLCβ, Gαq, and CSP are also known to regulate Cav2-type channels directly, and this possibility, as well as others, are discussed as mechanisms underlying their roles in homeostatic potentiation. Chapter 3 of this thesis reports the extended findings from expression of a gain-of-function Cav2-type channel. The Cav2.1 channel in humans is known to cause a dominant, heritable form of migraine called familial hemiplegic migraine (FHM). Two amino-acid substitutions causative for migraine were cloned into their analogous residues of the Drosophila Cav2 homolog. Expression of these migraine-modeled channels gave rise to several forms of hyperexcitability. Hyperexcitability defects included abnormal evoked waveforms, generation of spontaneous action potential-like events, and multi-quantal release. It is shown that these forms of hyperexcitability can be mitigated through targeted down-regulation of the PLCβ-IP3R-RyR intracellular signaling pathway. Chapter 4 presents an extended discussion as to the roles for presynaptic calcium channels, PLCβ, and CSP in homeostatic synaptic potentiation, and the mechanism underlying hyperexcitability downstream of gain-of-function Cav2-type channels. The proposed model aims to bridge the involvement of the PLCβ pathway in both homeostatic potentiation and neuronal excitability. Last, the implications for these findings on human disease conditions are elucidated.
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Campion, Katherine. "Characterisation of calcium-sensing receptor extracellular pH sensitivity and intracellular signal integration." Thesis, University of Manchester, 2013. https://www.research.manchester.ac.uk/portal/en/theses/characterisation-of-calciumsensing-receptor-extracellular-ph-sensitivity-and-intracellular-signal-integration(e11adf01-4748-42ed-8679-f8b990d79dea).html.

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Parathyroid hormone (PTH) secretion maintains free-ionised extracellular calcium (Ca2+o) homeostasis under the control of the calcium-sensing receptor (CaR). In humans and dogs, blood acidosis and alkalosis is associated with increased or suppressed PTH secretion respectively. Furthermore, large (1.0 pH unit) changes in extracellular pH (pHo) alter Ca2+o sensitivity of the CaR in CaR-transfected HEK-293 cells (CaR-HEK). Indeed, it has been found in this laboratory that even pathophysiological acidosis (pH 7.2) renders CaR less sensitive to Ca2+o while pathophysiological alkalosis (pH 7.6) increases its Ca2+o sensitivity, both in CaR-HEK and parathyroid cells. If true in vivo, then CaR’s pHo sensitivity might represent a mechanistic link between metabolic acidosis and hyperparathyroidism in ageing and renal disease. However, in acidosis one might speculate that the additional H+ could displace Ca2+ bound to plasma albumin, thus increasing free-Ca2+ concentration and so compensating for the decreased CaR responsiveness. Therefore, I first demonstrated that a physiologically-relevant concentration of albumin (5% w/v) failed to overcome the inhibitory effect of pH 7.2 or stimulatory effect of pH 7.6 on CaR-induced intracellular Ca2+ (Ca2+i) mobilisation. Determining the molecular basis of CaR pHo sensitivity would help explain cationic activation of CaR and permit the generation of experimental CaR models that specifically lack pHo sensitivity. With extracellular histidine and free cysteine residues the most likely candidates for pHo sensing (given their sidechains’ pK values), all 17 such CaR residues were mutated to non-ionisable residues. However, none of the resulting CaR mutants exhibited significantly decreased CaR pHo sensitivity. Even co-mutation of the two residues whose individual mutation appeared to elicit modest reductions (CaRH429V and CaRH495V) failed to exhibit any change in CaR pHo sensitivity. I conclude therefore, that neither extracellular histidine nor free cysteine residues account for CaR pHo sensitivity. Next, it is known that cytosolic cAMP drives PTH secretion in vivo and that cAMP potentiates Ca2+o-induced Ca2+i mobilisation in CaR-HEK cells. Given the physiological importance of tightly controlled PTH secretion and Ca2+o homeostasis, here I investigated the influence of cAMP on CaR signalling in CaR-HEK cells. Agents that increase cytosolic cAMP levels such as forskolin and isoproterenol potentiated Ca2+o-induced Ca2+i mobilisation and lowered the Ca2+o threshold for Ca2+i mobilisation. Indeed, forskolin lowered the EC50 for Ca2+o on CaR (2.3 ± 0.1 vs. 3.0 ± 0.1 mM control, P<0.001). Forskolin also potentiated CaR-induced ERK phosphorylation; however protein kinase A activation appeared uninvolved in any of these effects. Pertussis toxin, used to block CaR-induced suppression of cAMP accumulation, also lowered the Ca2+o threshold for Ca2+i mobilisation though appeared to do so by increasing efficacy (Emax). Furthermore, mutation of the CaR’s two putative PKA consensus sequences (CaRS899 and CaRS900) to a non-phosphorylatable residue (alanine) failed to alter the potency of Ca2+o for CaR or attenuate the forskolin response. In contrast, phosphomimetic mutation of CaRS899 (to aspartate) did increase CaR sensitivity to Ca2+o. Together this suggests that PKA-mediated CaRS899 phosphorylation could potentiate CaR activity but that this does not occur following Ca2+o treatment in CaR-HEK cells. Together, these data show that cAMP regulates the Ca2+o threshold for Ca2+i mobilisation, thus helping to explain differential efficacy between CaR downstream signals. If true in vivo, this could help explain how multiple physiological signal inputs may be integrated in parathyroid cells.
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Rintoul, Gordon Leslie. "Functional studies of calbindin-D¦2¦8[subscript]k and its role in intracellular calcium homeostasis." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/NQ61165.pdf.

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Hung, Chun-hin, and 孔進軒. "Effect of novel Chinese specific presenilin-1 V97L mutation on intracellular calcium homeostasis in human neuroblastoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/193533.

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Presenilin-1 (PS1) mutations caused by the PSEN1 gene mutations are the major cause of early onset familial Alzheimer’s disease (EOFAD). Two Chinesespecific EOFAD related PS1 mutations, V97L and A136G, have been found. Studies suggested that V97L mutation lead to the overexpression of Aβ42 and tau hyperphosphorylation, which are the major hallmarks of Alzheimer’s disease (AD), while properties of A136G were unclear. Since calcium dysregulation was suggested to play an important role in AD, the research project investigated if V97L and A136G mutations also lead to altered endoplasmic reticulum (ER) 〖Ca〗^(2+) regulation. SH-SY5Y cells transduced with retrovirus carrying V97L mutant or A136 mutant PSEN1 were used as the experiment models. In Western blotting, while the PS1 expression level was unaffected in V97L mutant, the expression level was significantly lower in A136G mutant. In carbachol (CCh) perfusion experiment, V97L mutant was found to exaggerate ER 〖Ca〗^(2+) release when stimulated by higher concentration (30, 100 and 300 μM) CCh, while A136G mutant exaggerated ER Ca2+ release when stimulated by 30 μM and 300 μM CCh, but not 100 μM CCh. In 5% fetal bovine serum (FBS) perfusion experiment, both V97L and A136G mutants were found to sensitize 〖Ca〗^(2+) oscillation, which the sensitization effect of V97L was 3 folds of A136G. The results suggested that V97L mutation exaggerates ER 〖Ca〗^(2+) release, possibly via interaction with IP3R. However the results of A136G were inconclusive and contradicting, therefore further investigation is needed.
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Gupta, Paul. "The control of intracellular calcium homeostasis by aspirin-like drugs and its relationship to mediator function." Thesis, University of Sunderland, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.237813.

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Books on the topic "Intracellular calcium homeostasis"

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Pansu, Danielle, and Felix Bronner, eds. Calcium Transport and Intracellular Calcium Homeostasis. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-83977-1.

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Danielle, Pansu, Bronner Felix, and North Atlantic Treaty Organization. Scientific Affairs Division., eds. Calcium transport and intracellular calcium homeostasis. Berlin: Springer-Verlag, 1990.

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Antonio, Rosado Juan, and SpringerLink (Online service), eds. Apoptosis: Involvement of Oxidative Stress and Intracellular Ca2+ Homeostasi. Dordrecht: Springer Netherlands, 2009.

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Bronner, Felix, and Danielle Pansu. Calcium Transport and Intracellular Calcium Homeostasis. Springer London, Limited, 2011.

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Bronner, Felix, and Danielle Pansu. Calcium Transport and Intracellular Calcium Homeostasis. Springer London, Limited, 2013.

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Pansu, D., and F. Bronner. Calcium Transport and Intracellular Calcium Homeostasis: Proceedings of the NATO Advanced Research Workshop on Calcium Transport and Intracellular Cal (NATO ASI series). Springer-Verlag, 1991.

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Rosengart, Matthew R. Disorders of calcium in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0253.

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Calcium is vitally important for normal cellular signalling and function. However, its toxicity necessitates that intracellular calcium concentration [Ca2+] be tightly regulated and compartmentalized. Evolutionary pressures have yielded several regulatory mechanisms to maintain intracellular and extracellular ionized calcium concentrations compatible with life. During periods of critical illness these process are commonly overwhelmed, and disorders of calcium homeostasis are highly prevalent among intensive care unit (ICU) patients. Indeed, hypocalcaemia occurs in up to 88% of critically-ill ICU patients suffering from trauma, sepsis, and burns. Contemporary evidence suggests that although hypocalcaemia may be associated with ICU mortality, it is not in the causal pathway. A systematic review concluded there are no data to support the routine parenteral administration of calcium in the management of asymptomatic critical illness-related hypocalcaemia. Asymptomatic hypocalcaemia of critical illness does not necessitate replacement. However, acute, symptomatic hypocalcaemia necessitates parenteral supplementation to prevent tetany, seizures, and cardiac arrhythmias
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Hahn, Robert G. Fluid and electrolyte physiology in anaesthetic practice. Edited by Jonathan G. Hardman. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0003.

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The maintenance of body fluid homeostasis is an essential task in perioperative care. Body fluid volumes are tightly controlled by the nervous system, by hormones, and by the kidneys. All these systems are affected by anaesthesia and surgery in ways that must be appreciated by the anaesthetist. Administration of infusion fluids is the key tool to prevent major derangements of the body fluid volumes during before, during, and after surgery. By varying its composition, an infusion fluid can be made to selectively expand or shrink a body fluid compartment. The total osmolality determines whether the infused volume distributes over the total body water or over the extracellular fluid volume, or even attracts fluid from intracellular space. Infusion fluid is the first-line tool in the management of the vasodilation that is induced by both general and regional anaesthesia. Fluids are also an essential component in the treatment of haemorrhage, in which a reduction in arterial pressure implies that 20% of the blood volume has been lost. Capillary refill restores the blood volume, but too slowly to prevent haemorrhagic shock. In this situation, prompt intravenous fluid therapy is life-saving. Electrolyte derangements may be induced by disease and/or medication. The most essential ones to consider during anaesthesia are sodium, potassium, calcium, and bicarbonate.
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Kwan, Melodie. Effect of the mood stabilizer valproate on intracellular calcium homeostatis in bipolar I disorder. 2004.

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Book chapters on the topic "Intracellular calcium homeostasis"

1

Miller, Richard J. "Modulation and Functions of Neuronal Ca2+ Permeable Channels." In Calcium Transport and Intracellular Calcium Homeostasis, 3–17. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-83977-1_1.

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Walters, Julian R. F. "The Activity of the Basolateral Membrane Calcium-Pumping ATPase and Intestinal Calcium Transport." In Calcium Transport and Intracellular Calcium Homeostasis, 95–101. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-83977-1_10.

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Reeves, John P., Diane C. Ahrens, Joo Cheon, and John T. Durkin. "Sodium-Calcium Exchange in the Heart." In Calcium Transport and Intracellular Calcium Homeostasis, 105–21. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-83977-1_11.

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Blaustein, M. P., S. Bova, X. J. Yuan, and W. F. Goldman. "The Role of Sodium/Calcium Exchange in the Regulation of Vascular Contractility." In Calcium Transport and Intracellular Calcium Homeostasis, 123–32. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-83977-1_12.

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Windhager, E. E. "Function and Regulation of Intracellular Ca in Renal Cells." In Calcium Transport and Intracellular Calcium Homeostasis, 135–48. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-83977-1_13.

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Borle, André B. "Na+-Ca2+ and Na+-H+ Antiporter Interactions. Relations between Cytosolic Free Ca2+, Na+ and Intracellular pH." In Calcium Transport and Intracellular Calcium Homeostasis, 149–59. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-83977-1_14.

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Lang, F., M. Paulmichl, F. Friedrich, J. Pfeilschifter, E. Woell, and H. Weiss. "Regulation of Intracellular Calcium in Cultured Renal Epithelioid (MDCK-) Cells." In Calcium Transport and Intracellular Calcium Homeostasis, 161–68. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-83977-1_15.

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Downey, G. P., S. Trudel, W. Furuya, and S. Grinstein. "Assessment of the Role of Calcium in Neutrophil Activation Using Electropermeabilized Cells." In Calcium Transport and Intracellular Calcium Homeostasis, 169–76. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-83977-1_16.

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Lau, K. R., and R. M. Case. "The Role of Calcium in Regulating the Agonist-Evoked Intracellular Acidosis in Rabbit Salivary Gland Acini." In Calcium Transport and Intracellular Calcium Homeostasis, 177–84. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-83977-1_17.

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Vincenzi, Frank F., Thomas R. Hinds, and Armando Lindner. "Free Calcium in Red Blood Cells of Human Hypertensives is Elevated: How Can This be?" In Calcium Transport and Intracellular Calcium Homeostasis, 185–95. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-83977-1_18.

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Conference papers on the topic "Intracellular calcium homeostasis"

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Sheikh, Abdul Q., Jennifer R. Hurley, and Daria A. Narmoneva. "Diabetes Alters Intracellular Calcium Transients in Cardiac Endothelial Cells." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53797.

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Diabetic cardiomyopathy (DCM) is a serious diabetes-associated complication that results in myocardial dysfunction independent of other etiological factors [1]. Pathological alterations to the myocardium associated with DCM include circulatory defects, impaired heart muscle contraction, and abnormal calcium (Ca2+) homeostasis in cardiac cells[2]. In myocardium, endothelial cells play an essential role in maintaining intracellular Ca2+ hemostasis in response to stimuli and regulating cardiac function [3]. External stimulus may cause abrupt changes in Ca2+ balance, including Ca2+ release from sarco-endoplasmic reticulum (ER) [4]. Subsequent return of the Ca2+ level to basal levels occurs due to Ca2+ decay mechanism, which is mainly regulated by sarco-endoplasmic reticulum Ca2+ ATPase pumps (SERCA) present at ER membrane which are responsible for Ca2+ sequestration [5]. Studies have shown that the mechanisms by which Ca2+ homeostasis alters cardiac function in diabetic cardiomyocytes include reduced activity of the SERCA pumps [6]. However, no information is available regarding the effects of diabetes on Ca2+ hemostasis and the underlying Ca2+ sequestration mechanism in diabetic cardiac endothelial cells[7]. This study tested the hypothesis that diabetic endothelial cells will exhibit disruptions in Ca2+ decay kinetics via alterations in the sequestration mechanism.
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Erickson, Geoffrey R., and Farshid Guilak. "Osmotic Stress Initiates Intracellular Calcium Waves in Chondrocytes Through Extracellular Influx and the Inositol Phosphate Pathway." In ASME 1999 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1999. http://dx.doi.org/10.1115/imece1999-0580.

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Abstract The biophysical environment of the chondrocytes plays an important role in the health, turnover, and homeostasis of articular cartilage. Under normal physiologic loading, chondrocytes are exposed to a complex and diverse array of biophysical signals, including mechanical and osmotic stresses, fluid flow, and fluid pressures [4]. Due to the charged and hydrated nature of the extracellular matrix, mechanical compression causes exudation of interstitial fluid in cartilage, which alters the osmotic environment of the chondrocytes. Confocal microscopy studies have shown that chondrocytes lose or gain volume in response to tissue compression [4] or changes in extracellular osmolarity [3]. The active process of volume recovery subsequent to osmotic shock has been shown to initiate intracellular signaling cascades [2], which may in turn alter cellular metabolism [6]. Although the mechanisms of intracellular signaling in response to osmotic stress are not fully understood, it has been hypothesized that intracellular transients and oscillations of calcium ion (Ca2+) are involved. The objective of this study was to examine the hypothesis that osmotic stress initiates a transient increase in the concentration of intracellular calcium ion ([Ca2+]i), and to determine the mechanisms of Ca2+ mobilization in isolated chondrocytes exposed to hypo- and hyper-osmotic stress.
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Bukowski, Michael, Brij Singh, James Roemmich, and Kate Larson. "Lipidomic analysis of TRPC1 Ca2+-permeable channel-knock out mouse demonstrates a vital role in placental tissue sphingolipid and triacylglycerol homeostasis under high-fat diet." In 2022 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2022. http://dx.doi.org/10.21748/tjdt4839.

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Placental function including oxygen delivery and nutrient transport are critical determinants of fetal growth, moderating the risks of obesity and metabolic diseases later in life. Previously, we demonstrated in a mouse model that parental diet and exercise play important roles in placental lipid content and inflammation. Transient receptor potential canonical channel 1 (TRPC1) is a Ca2+-permeable integral membrane protein. We have demonstrated that TRPC1 increases total body adiposity in mice by decreasing the efficacy of exercise to limit adipose accumulation under a high fat (HF) diet. Importantly, intracellular calcium may regulate total body adiposity and increased total body adiposity could promote placental lipid accumulation. Similarly, intracellular calcium regulates membrane lipid content via the activation of the protein kinase C. Membrane lipids such as sphingomyelin are key regulators of cell signaling. Maternal HF diets increase placental tissue lipid concentrations resulting in compromised nutrient transport to fetus. However, the specific lipid species that accumulate due to the absence of the placental TRPC1 gene under maternal HF diet feeding is not yet known. We hypothesized that placental tissue response to a maternal HF diet is disrupted in TRPC1 mice fed a maternal HF diet resulting in greater cellular sphingomyelin concentrations. Results showed placentae from TRPC1 KO mice fed high fat diet (45% en, HF) had increased sphingomyelin concentrations compared to control diet (16% en, NF). Placentae from WT mice fed HF diet exhibited diet-dependent increases in ceramide concentration with no concomitant increase in sphingomyelins compared to NF fed WT mice. Additionally, 11 placental triacylglycerol (TAG) species were different based on diet, 16 based on genotype, and 5 were affected by both diet and genotype. These results suggest that during a HF diet, loss of TRPC1 function reduces placental sphingomyelin hydrolysis into ceramide and that placental TAG concentrations respond in diet- and genotype-dependent manner.
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She, Yue, Zhong Wang, Nan Wang, and Yanfei Li. "Notice of Retraction: Effects of Aluminum on Intracellular Calcium Homeostasis of Splenic Lymphocytes in Chickens Cultured In Vitro: Preliminary Study of Aluminum Immunotoxicity in Chickens." In 2011 5th International Conference on Bioinformatics and Biomedical Engineering. IEEE, 2011. http://dx.doi.org/10.1109/icbbe.2011.5781428.

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Reports on the topic "Intracellular calcium homeostasis"

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Sosa Munguía, Paulina del Carmen, Verónica Ajelet Vargaz Guadarrama, Marcial Sánchez Tecuatl, Mario Garcia Carrasco, Francesco Moccia, and Roberto Berra-Romani. Diabetes mellitus alters intracellular calcium homeostasis in vascular endothelial cells: a systematic review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2022. http://dx.doi.org/10.37766/inplasy2022.5.0104.

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Review question / Objective: What are the effects of diabetes mellitus on the calcium homeostasis in vascular endothelial cells? -To describe the effects of diabetes on the mechanisms that regulate intracellular calcium; -To describe other molecules/mechanisms that alters intracellular Ca2+ homeostasis. Condition being studied: Diabetes mellitus is a pathology with a high incidence in the population, characterized by an increase in blood glucose. People with diabetes are 2-4 times more likely to suffer from a cardiovascular complication, such as total or partial loss of sight, myocardial infarction, kidney failure, among others. Cardiovascular complications have been reported to derive from dysfunction of endothelial cells, which have important functions in blood vessels. In order to understand the etiology of this poor function of endothelial cells, it is necessary to study the molecular mechanisms involved in these functions, to identify the effects of diabetes and thus, develop new research that will mitigate the effects of this pathology.
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