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1
Penner, R., and E. Neher. "The role of calcium in stimulus-secretion coupling in excitable and non-excitable cells." Journal of Experimental Biology 139, no. 1 (1988): 329–45. http://dx.doi.org/10.1242/jeb.139.1.329.
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Secretion of vesicular contents by exocytosis is a common feature of excitable (neurones, chromaffin cells, beta cells) and non-excitable cells (platelets, neutrophils, mast cells). The simplistic view that the universal mechanism controlling secretion is elevation of [Ca2+]i--whatever the source of this second messenger may be--is no longer tenable in view of recent reports demonstrating secretion at basal or even reduced [Ca2+]i. It is nevertheless clear that in excitable cells an increase in [Ca2+]i is the triggering event that induces secretion. In non-excitable cells, secretion is presumably triggered by other second messengers, although [Ca2+]i appears to act as an important modulator of the rate of secretion. Conversely, these second messenger systems may serve a regulatory function in excitable cells. Given the relative importance of [Ca2+]i in the regulation of cellular functions in excitable and non-excitable cells, it is not surprising that several mechanisms are expressed in these cells to regulate intracellular calcium concentration. The major pathway for Ca2+ in excitable cells is by voltage-activated Ca2+ channels, but release of Ca2+ from intracellular stores, via second messengers, predominates in non-excitable cells, and may also be important in excitable cells. In addition, receptor-operated channels and second messenger-gated conductances may prove to be important. All of these pathways are subject to regulation by a variety of interactive second messenger systems, which provide necessary tuning for an appropriate control of intracellular calcium level.
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Praetorius, Helle A., and Jens Leipziger. "ATP release from non-excitable cells." Purinergic Signalling 5, no. 4 (2009): 433–46. http://dx.doi.org/10.1007/s11302-009-9146-2.
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Sanhueza, Dayán, Andro Montoya, Jimena Sierralta, and Manuel Kukuljan. "Expression of voltage-activated calcium channels in the early zebrafish embryo." Zygote 17, no. 2 (2009): 131–35. http://dx.doi.org/10.1017/s0967199408005108.
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SummaryIncreases in cytosolic calcium concentrations regulate many cellular processes, including aspects of early development. Calcium release from intracellular stores and calcium entry through non-voltage-gated channels account for signalling in non-excitable cells, whereas voltage-gated calcium channels (CaV) are important in excitable cells. We report the expression of multiple transcripts of CaV, identified by its homology to other species, in the early embryo of the zebrafish, Danio rerio, at stages prior to the differentiation of excitable cells. CaV mRNAs and proteins were detected as early as the 2-cell stages, which indicate that they arise from both maternal and zygotic transcription. Exposure of embryos to pharmacological blockers of CaV does not perturb early development significantly, although late effects are appreciable. These results suggest that CaV may have a role in calcium homeostasis and control of cellular process during early embryonic development.
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Sukumaran, Pramod, Viviane Nascimento Da Conceicao, Yuyang Sun, et al. "Calcium Signaling Regulates Autophagy and Apoptosis." Cells 10, no. 8 (2021): 2125. http://dx.doi.org/10.3390/cells10082125.
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Calcium (Ca2+) functions as a second messenger that is critical in regulating fundamental physiological functions such as cell growth/development, cell survival, neuronal development and/or the maintenance of cellular functions. The coordination among various proteins/pumps/Ca2+ channels and Ca2+ storage in various organelles is critical in maintaining cytosolic Ca2+ levels that provide the spatial resolution needed for cellular homeostasis. An important regulatory aspect of Ca2+ homeostasis is a store operated Ca2+ entry (SOCE) mechanism that is activated by the depletion of Ca2+ from internal ER stores and has gained much attention for influencing functions in both excitable and non-excitable cells. Ca2+ has been shown to regulate opposing functions such as autophagy, that promote cell survival; on the other hand, Ca2+ also regulates programmed cell death processes such as apoptosis. The functional significance of the TRP/Orai channels has been elaborately studied; however, information on how they can modulate opposing functions and modulate function in excitable and non-excitable cells is limited. Importantly, perturbations in SOCE have been implicated in a spectrum of pathological neurodegenerative conditions. The critical role of autophagy machinery in the pathogenesis of neurodegenerative diseases such as Alzheimer’s, Parkinson’s, and Huntington’s diseases, would presumably unveil avenues for plausible therapeutic interventions for these diseases. We thus review the role of SOCE-regulated Ca2+ signaling in modulating these diverse functions in stem cell, immune regulation and neuromodulation.
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Bai, Xilian, George J. Bugg, Susan L. Greenwood, et al. "Expression of TASK and TREK, two-pore domain K+ channels, in human myometrium." Reproduction 129, no. 4 (2005): 525–30. http://dx.doi.org/10.1530/rep.1.00442.
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Two-pore domain K+channels are an emerging family of K+channels that may contribute to setting membrane potential in both electrically excitable and non-excitable cells and, as such, influence cellular function. The human uteroplacental unit contains both excitable (e.g. myometrial) and non-excitable cells, whose function depends upon the activity of K+channels. We have therefore investigated the expression of two members of this family, TWIK (two-pore domain weak inward rectifying K+channel)-related acid-sensitive K+channel (TASK) and TWIK-related K+channel (TREK) in human myometrium. Using RT-PCR the mRNA expression of TASK and TREK isoforms was examined in myometrial tissue from pregnant women. mRNAs encoding TASK1, 4 and 5 and TREK1 were detected whereas weak or no signals were observed for TASK2, TASK3 and TREK2. Western blotting for TASK1 gave two bands of approximately 44 and 65 kDa, whereas TREK1 gave bands of approximately 59 and 90 kDa in myometrium from pregnant women. TASK1 and TREK1 immunofluorescence was prominent in intracellular and plasmalemmal locations within myometrial cells. Therefore, we conclude that the human myometrium is a site of expression for the two-pore domain K+channel proteins TASK1 and TREK1.
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Beaumont, V. "Visualizing membrane trafficking using total internal reflection fluorescence microscopy." Biochemical Society Transactions 31, no. 4 (2003): 819–23. http://dx.doi.org/10.1042/bst0310819.
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There is a dizzying array of fluorescent probes now commercially available to monitor cellular processes, and advances in molecular biology have highlighted the ease with which proteins can now be labelled with fluorophores without loss of functionality. This has led to an explosion in the popularity of fluorescence microscopy techniques. One such specialized technique, total internal reflection fluorescence microscopy (TIR-FM), is ideally suited to gaining insight into events occurring at, or close to, the plasma membrane of live cells with excellent optical resolution. In the last few years, the application of TIR-FM to membrane trafficking events in both non-excitable and excitable cells has been an area of notable expansion and fruition. This review gives a brief overview of that literature, with emphasis on the study of the regulation of exocytosis and endocytosis in excitable cells using TIR-FM. Finally, recent applications of TIR-FM to the study of cellular processes at the molecular level are discussed briefly, providing promise that the future of TIR-FM in cell biology will only get brighter.
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Sargsyan, Yelena, Uta Bickmeyer, Christine S. Gibhardt, Katrin Streckfuss-Bömeke, Ivan Bogeski, and Sven Thoms. "Peroxisomes contribute to intracellular calcium dynamics in cardiomyocytes and non-excitable cells." Life Science Alliance 4, no. 9 (2021): e202000987. http://dx.doi.org/10.26508/lsa.202000987.
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Peroxisomes communicate with other cellular compartments by transfer of various metabolites. However, whether peroxisomes are sites for calcium handling and exchange has remained contentious. Here we generated sensors for assessment of peroxisomal calcium and applied them for single cell-based calcium imaging in HeLa cells and cardiomyocytes. We found that peroxisomes in HeLa cells take up calcium upon depletion of intracellular calcium stores and upon calcium influx across the plasma membrane. Furthermore, we show that peroxisomes of neonatal rat cardiomyocytes and human induced pluripotent stem cell–derived cardiomyocytes can take up calcium. Our results indicate that peroxisomal and cytosolic calcium signals are tightly interconnected both in HeLa cells and in cardiomyocytes. Cardiac peroxisomes take up calcium on beat-to-beat basis. Hence, peroxisomes may play an important role in shaping cellular calcium dynamics of cardiomyocytes.
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Bettendorff, Lucien. "Thiamine in excitable tissues: Reflections on a non-cofactor role." Metabolic Brain Disease 9, no. 3 (1994): 183–209. http://dx.doi.org/10.1007/bf01991194.
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Verkhratsky, Alexei, and Maiken Nedergaard. "The homeostatic astroglia emerges from evolutionary specialization of neural cells." Philosophical Transactions of the Royal Society B: Biological Sciences 371, no. 1700 (2016): 20150428. http://dx.doi.org/10.1098/rstb.2015.0428.
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Evolution of the nervous system progressed through cellular diversification and specialization of functions. Conceptually, the nervous system is composed from electrically excitable neuronal networks connected with chemical synapses and non-excitable glial cells that provide for homeostasis and defence. Astrocytes are integrated into neural networks through multipartite synapses; astroglial perisynaptic processes closely enwrap synaptic contacts and control homeostasis of the synaptic cleft, supply neurons with glutamate and GABA obligatory precursor glutamine and contribute to synaptic plasticity, learning and memory. In neuropathology, astrocytes may undergo reactive remodelling or degeneration; to a large extent, astroglial reactions define progression of the pathology and neurological outcome. This article is part of the themed issue ‘Evolution brings Ca 2+ and ATP together to control life and death’.
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Chu, Jun, Russell D. Haynes, Stéphane Y. Corbel, et al. "Non-invasive intravital imaging of cellular differentiation with a bright red-excitable fluorescent protein." Nature Methods 11, no. 5 (2014): 572–78. http://dx.doi.org/10.1038/nmeth.2888.
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Kraus, Michael, and Bernhard Wolf. "Mathematical Model for Agonist-Induced Oscillatory Calcium Waves in Non-Excitable Mammalian Cells." Neurosignals 1, no. 2 (1992): 101–13. http://dx.doi.org/10.1159/000109316.
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Falcón, Débora, Isabel Galeano-Otero, Marta Martín-Bórnez, et al. "TRPC Channels: Dysregulation and Ca2+ Mishandling in Ischemic Heart Disease." Cells 9, no. 1 (2020): 173. http://dx.doi.org/10.3390/cells9010173.
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Transient receptor potential canonical (TRPC) channels are ubiquitously expressed in excitable and non-excitable cardiac cells where they sense and respond to a wide variety of physical and chemical stimuli. As other TRP channels, TRPC channels may form homo or heterotetrameric ion channels, and they can associate with other membrane receptors and ion channels to regulate intracellular calcium concentration. Dysfunctions of TRPC channels are involved in many types of cardiovascular diseases. Significant increase in the expression of different TRPC isoforms was observed in different animal models of heart infarcts and in vitro experimental models of ischemia and reperfusion. TRPC channel-mediated increase of the intracellular Ca2+ concentration seems to be required for the activation of the signaling pathway that plays minor roles in the healthy heart, but they are more relevant for cardiac responses to ischemia, such as the activation of different factors of transcription and cardiac hypertrophy, fibrosis, and angiogenesis. In this review, we highlight the current knowledge regarding TRPC implication in different cellular processes related to ischemia and reperfusion and to heart infarction.
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Cojocaru, Alexandru, Emilia Burada, Adrian-Tudor Bălșeanu, et al. "Roles of Microglial Ion Channel in Neurodegenerative Diseases." Journal of Clinical Medicine 10, no. 6 (2021): 1239. http://dx.doi.org/10.3390/jcm10061239.
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As the average age and life expectancy increases, the incidence of both acute and chronic central nervous system (CNS) pathologies will increase. Understanding mechanisms underlying neuroinflammation as the common feature of any neurodegenerative pathology, we can exploit the pharmacology of cell specific ion channels to improve the outcome of many CNS diseases. As the main cellular player of neuroinflammation, microglia play a central role in this process. Although microglia are considered non-excitable cells, they express a variety of ion channels under both physiological and pathological conditions that seem to be involved in a plethora of cellular processes. Here, we discuss the impact of modulating microglia voltage-gated, potential transient receptor, chloride and proton channels on microglial proliferation, migration, and phagocytosis in neurodegenerative diseases.
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Gilmore, Stephen, and Kerry A. Landman. "Is the Skin an Excitable Medium? Pattern Formation in Erythema Gyratum Repens." Journal of Theoretical Medicine 6, no. 1 (2005): 57–65. http://dx.doi.org/10.1080/10273660500066618.
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Erythema gyratum repens (EGR) is a rare, inflammatory dermatosis of unknown aetiology. The morphology of the eruption is striking and displays rapidly evolving circinate and gyrate bands of erythematous and scaly skin. Although the aetiology of the pattern is unknown, it has previously been noted that the eruption shares morphologic features with the patterns of spatio-temporal chemical concentration profiles observed in the Belusov-Zhabotinski (BZ) reaction. Yet this morphologic correspondence has not been investigated further. Here we apply a simple non-linear reaction–diffusion model, previously used to describe the BZ reaction, as a template for pattern formation in EGR, and show how the mechanism may provide a biochemical basis for many of the dynamic and morphologic features of the rash. These results are supported by the results of a cellular automaton simulation approximating the dynamics of oscillatory chemical systems—the Hodgepodge machine—where the spatio-temporal patterns developed show astonishing similarities to the morphology of EGR.
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Totland, Max Zachrisson, Nikoline Lander Rasmussen, Lars Mørland Knudsen, and Edward Leithe. "Regulation of gap junction intercellular communication by connexin ubiquitination: physiological and pathophysiological implications." Cellular and Molecular Life Sciences 77, no. 4 (2019): 573–91. http://dx.doi.org/10.1007/s00018-019-03285-0.
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Abstract Gap junctions consist of arrays of intercellular channels that enable adjacent cells to communicate both electrically and metabolically. Gap junctions have a wide diversity of physiological functions, playing critical roles in both excitable and non-excitable tissues. Gap junction channels are formed by integral membrane proteins called connexins. Inherited or acquired alterations in connexins are associated with numerous diseases, including heart failure, neuropathologies, deafness, skin disorders, cataracts and cancer. Gap junctions are highly dynamic structures and by modulating the turnover rate of connexins, cells can rapidly alter the number of gap junction channels at the plasma membrane in response to extracellular or intracellular cues. Increasing evidence suggests that ubiquitination has important roles in the regulation of endoplasmic reticulum-associated degradation of connexins as well as in the modulation of gap junction endocytosis and post-endocytic sorting of connexins to lysosomes. In recent years, researchers have also started to provide insights into the physiological roles of connexin ubiquitination in specific tissue types. This review provides an overview of the advances made in understanding the roles of connexin ubiquitination in the regulation of gap junction intercellular communication and discusses the emerging physiological and pathophysiological implications of these processes.
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Dagan, Inbal, and Raz Palty. "Regulation of Store-Operated Ca2+ Entry by SARAF." Cells 10, no. 8 (2021): 1887. http://dx.doi.org/10.3390/cells10081887.
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Calcium (Ca2+) signaling plays a dichotomous role in cellular biology, controlling cell survival and proliferation on the one hand and cellular toxicity and cell death on the other. Store-operated Ca2+ entry (SOCE) by CRAC channels represents a major pathway for Ca2+ entry in non-excitable cells. The CRAC channel has two key components, the endoplasmic reticulum Ca2+ sensor stromal interaction molecule (STIM) and the plasma-membrane Ca2+ channel Orai. Physical coupling between STIM and Orai opens the CRAC channel and the resulting Ca2+ flux is regulated by a negative feedback mechanism of slow Ca2+ dependent inactivation (SCDI). The identification of the SOCE-associated regulatory factor (SARAF) and investigations of its role in SCDI have led to new functional and molecular insights into how SOCE is controlled. In this review, we provide an overview of the functional and molecular mechanisms underlying SCDI and discuss how the interaction between SARAF, STIM1, and Orai1 shapes Ca2+ signaling in cells.
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Le Guilcher, Camille, Tomas Luyten, Jan B. Parys, Mathieu Pucheault, and Olivier Dellis. "Synthesis and Characterization of Store-Operated Calcium Entry Inhibitors Active in the Submicromolar Range." International Journal of Molecular Sciences 21, no. 24 (2020): 9777. http://dx.doi.org/10.3390/ijms21249777.
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The store-operated calcium entry, better known as SOCE, forms the main Ca2+ influx pathway in non-excitable cells, especially in leukocytes, where it is required for cell activation and the immune response. During the past decades, several inhibitors were developed, but they lack specificity or efficacy. From the non-specific SOCE inhibitor 2-aminoethyl diphenylborinate (2-APB), we synthetized 16 new analogues by replacing/modifying the phenyl groups. Among them, our compound P11 showed the best inhibitory capacity with a Ki ≈ 75 nM. Furthermore, below 1 µM, P11 was devoid of any inhibitory activity on the two other main cellular targets of 2-APB, the IP3 receptors, and the SERCA pumps. Interestingly, Jurkat T cells secrete interleukin-2 under phytohemagglutinin stimulation but undergo cell death and stop IL-2 synthesis when stimulated in the presence of increasing P11 concentrations. Thus, P11 could represent the first member of a new and potent family of immunosuppressors.
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Chapotte-Baldacci, Charles-Albert, Guénaëlle Lizot, Cyrielle Jajkiewicz, et al. "Fine Tuning of Calcium Constitutive Entry by Optogenetically-Controlled Membrane Polarization: Impact on Cell Migration." Cells 9, no. 7 (2020): 1684. http://dx.doi.org/10.3390/cells9071684.
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Anomalies in constitutive calcium entry (CCE) have been commonly attributed to cell dysfunction in pathological conditions such as cancer. Calcium influxes of this type rely on channels, such as transient receptor potential (TRP) channels, to be constitutively opened and strongly depend on membrane potential and a calcium driving force. We developed an optogenetic approach based on the expression of the halorhodopsin chloride pump to study CCE in non-excitable cells. Using C2C12 cells, we found that halorhodopsin can be used to achieve a finely tuned control of membrane polarization. Escalating the membrane polarization by incremental changes in light led to a concomitant increase in CCE through transient receptor potential vanilloid 2 (TRPV2) channels. Moreover, light-induced calcium entry through TRPV2 channels promoted cell migration. Our study shows for the first time that by modulating CCE and related physiological responses, such as cell motility, halorhodopsin serves as a potentially powerful tool that could open new avenues for the study of CCE and associated cellular behaviors.
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Bergmeier, Wolfgang, Masatsugu Oh-hora, Christie-Ann McCarl, R. Claire Roden, Paul F. Bray, and Stefan Feske. "R93W Mutation in Orai1 Causes Impaired Calcium Influx in Platelets." Blood 112, no. 11 (2008): 1838. http://dx.doi.org/10.1182/blood.v112.11.1838.1838.
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Abstract The intracellular Ca2+ concentration of non-excitable cells is regulated by calcium store release and store-operated calcium entry (SOCE). In platelets, STIM1 was recently identified as the main calcium sensor expressed in the endoplasmatic reticulum. To evaluate the role of the SOC channel moiety, Orai1, in platelet SOCE, we generated mice expressing a mutated, inactive form of Orai1 in blood cells only (Orai1R93W). Platelets expressing Orai1R93W were characterized by markedly reduced SOCE and impaired agonist-induced increases in [Ca2+]i. Orai1R93W platelets showed reduced integrin activation and impaired degranulation when stimulated with low agonist concentrations under static conditions. This defect, however, did not significantly affect the ability of Orai1R93W platelets to aggregate or to adhere to collagen under arterial flow conditions ex vivo. In contrast, these adherent Orai1R93W platelets were defective in surface phosphatidylserine exposure, suggesting that Orai1 is crucial for the platelets pro-coagulant response rather than for other Ca2+-dependent cellular responses.
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Etrych, Tomáš, Olga Janoušková, and Petr Chytil. "Fluorescence Imaging as a Tool in Preclinical Evaluation of Polymer-Based Nano-DDS Systems Intended for Cancer Treatment." Pharmaceutics 11, no. 9 (2019): 471. http://dx.doi.org/10.3390/pharmaceutics11090471.
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Targeted drug delivery using nano-sized carrier systems with targeting functions to malignant and inflammatory tissue and tailored controlled drug release inside targeted tissues or cells has been and is still intensively studied. A detailed understanding of the correlation between the pharmacokinetic properties and structure of the nano-sized carrier is crucial for the successful transition of targeted drug delivery nanomedicines into clinical practice. In preclinical research in particular, fluorescence imaging has become one of the most commonly used powerful imaging tools. Increasing numbers of suitable fluorescent dyes that are excitable in the visible to near-infrared (NIR) wavelengths of the spectrum and the non-invasive nature of the method have significantly expanded the applicability of fluorescence imaging. This chapter summarizes non-invasive fluorescence-based imaging methods and discusses their potential advantages and limitations in the field of drug delivery, especially in anticancer therapy. This chapter focuses on fluorescent imaging from the cellular level up to the highly sophisticated three-dimensional imaging modality at a systemic level. Moreover, we describe the possibility for simultaneous treatment and imaging using fluorescence theranostics and the combination of different imaging techniques, e.g., fluorescence imaging with computed tomography.
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Hammad, Ayat S., and Khaled Machaca. "Store Operated Calcium Entry in Cell Migration and Cancer Metastasis." Cells 10, no. 5 (2021): 1246. http://dx.doi.org/10.3390/cells10051246.
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Ca2+ signaling is ubiquitous in eukaryotic cells and modulates many cellular events including cell migration. Directional cell migration requires the polarization of both signaling and structural elements. This polarization is reflected in various Ca2+ signaling pathways that impinge on cell movement. In particular, store-operated Ca2+ entry (SOCE) plays important roles in regulating cell movement at both the front and rear of migrating cells. SOCE represents a predominant Ca2+ influx pathway in non-excitable cells, which are the primary migrating cells in multicellular organisms. In this review, we summarize the role of Ca2+ signaling in cell migration with a focus on SOCE and its diverse functions in migrating cells and cancer metastasis. SOCE has been implicated in regulating focal adhesion turnover in a polarized fashion and the mechanisms involved are beginning to be elucidated. However, SOCE is also involved is other aspects of cell migration with a less well-defined mechanistic understanding. Therefore, much remains to be learned regarding the role and regulation of SOCE in migrating cells.
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Cretoiu, Sanda M., Dragos Cretoiu, Adela Marin, Beatrice Mihaela Radu, and Laurentiu M. Popescu. "Telocytes: ultrastructural, immunohistochemical and electrophysiological characteristics in human myometrium." REPRODUCTION 145, no. 4 (2013): 357–70. http://dx.doi.org/10.1530/rep-12-0369.
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Telocytes (TCs) have been described in various organs and species (www.telocytes.com) as cells with telopodes (Tps) – very long cellular extensions with an alternation of thin segments (podomers) and dilated portions (podoms). We examined TCs using electron microscopy (EM), immunohistochemistry (IHC), immunofluorescence (IF), time-lapse videomicroscopy and whole-cell patch voltage clamp. EM showed a three-dimensional network of dichotomous-branching Tps, a labyrinthine system with homocellular and heterocellular junctions. Tps release extracellular vesicles (mean diameter of 160.6±6.9 nm in non-pregnant myometrium and 171.6±4.6 nm in pregnant myometrium), sending macromolecular signals to neighbouring cells. Comparative measurements (non-pregnant and pregnant myometrium) of podomer thickness revealed values of 81.94±1.77 vs 75.53±1.81 nm, while the podoms' diameters were 268.6±8.27 vs 316.38±17.56 nm. IHC as well as IF revealed double c-kit and CD34 positive results. Time-lapse videomicroscopy of cell culture showed dynamic interactions between Tps and myocytes. In non-pregnant myometrium, patch-clamp recordings of TCs revealed a hyperpolarisation-activated chloride inward current with calcium dependence and the absence of L-type calcium channels. TCs seem to have no excitable properties similar to the surrounding smooth muscle cells (SMCs). In conclusion, this study shows the presence of TCs as a distinct cell type in human non-pregnant and pregnant myometrium and describes morphometric differences between the two physiological states. In addition, we provide a preliminaryin vitroelectrophysiological evaluation of the non-pregnant state, suggesting that TCs could influence timing of the contractile activity of SMCs.
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REDONDO, Pedro C., Ana I. LAJAS, Ginés M. SALIDO, Antonio GONZALEZ, Juan A. ROSADO, and José A. PARIENTE. "Evidence for secretion-like coupling involving pp60src in the activation and maintenance of store-mediated Ca2+ entry in mouse pancreatic acinar cells." Biochemical Journal 370, no. 1 (2003): 255–63. http://dx.doi.org/10.1042/bj20021505.
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Store-mediated Ca2+ entry (SMCE) is one of the main pathways for Ca2+ influx in non-excitable cells. Recent studies favour a secretion-like coupling mechanism to explain SMCE, where Ca2+ entry is mediated by an interaction of the endoplasmic reticulum (ER) with the plasma membrane (PM) and is modulated by the actin cytoskeleton. To explore this possibility further we have now investigated the role of the actin cytoskeleton in the activation and maintenance of SMCE in pancreatic acinar cells, a more specialized secretory cell type which might be an ideal cellular model to investigate further the properties of the secretion-like coupling model. In these cells, the cytoskeletal disrupters cytochalasin D and latrunculin A inhibited both the activation and maintenance of SMCE. In addition, stabilization of a cortical actin barrier by jasplakinolide prevented the activation, but not the maintenance, of SMCE, suggesting that, as for secretion, the actin cytoskeleton plays a double role in SMCE as a negative modulator of the interaction between the ER and PM, but is also required for this mechanism, since the cytoskeleton disrupters impaired Ca2+ entry. Finally, depletion of the intracellular Ca2+ stores induces cytoskeletal association and activation of pp60src, which is independent on Ca2+ entry. pp60src activation requires the integrity of the actin cytoskeleton and participates in the initial phase of the activation of SMCE in pancreatic acinar cells.
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Lawrence, Gary W., Tomas H. Zurawski, and J. Oliver Dolly. "Ca2+ Signalling Induced by NGF Identifies a Subset of Capsaicin-Excitable Neurons Displaying Enhanced Chemo-Nociception in Dorsal Root Ganglion Explants from Adult pirt-GCaMP3 Mouse." International Journal of Molecular Sciences 22, no. 5 (2021): 2589. http://dx.doi.org/10.3390/ijms22052589.
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Nociceptors sense hazards via plasmalemmal cation channels, including transient receptor potential vanilloid 1 (TRPV1). Nerve growth factor (NGF) sensitises TRPV1 to capsaicin (CAPS), modulates nociceptor excitability and induces thermal hyperalgesia, but cellular mechanisms remain unclear. Confocal microscopy was used to image changes in intracellular Ca2+ concentration ([Ca2+]i) across neuronal populations in dorsal root ganglia (DRG) explants from pirt-GCaMP3 adult mice, which express a fluorescent reporter in their sensory neurons. Raised [Ca2+]i was detected in 84 neurons of three DRG explants exposed to NGF (100 ng/mL) and most (96%) of these were also excited by 1 μM CAPS. NGF elevated [Ca2+]i in about one-third of the neurons stimulated by 1 μM CAPS, whether applied before or after the latter. In neurons excitable by NGF, CAPS-evoked [Ca2+]i signals appeared significantly sooner (e.g., respective lags of 1.0 ± 0.1 and 1.9 ± 0.1 min), were much (>30%) brighter and lasted longer (6.6 ± 0.4 vs. 3.9 ± 0.2 min) relative to those non-responsive to the neurotrophin. CAPS tachyphylaxis lowered signal intensity by ~60% but was largely prevented by NGF. Increasing CAPS from 1 to 10 μM nearly doubled the number of cells activated but only modestly increased the amount co-activated by NGF. In conclusion, a sub-population of the CAPS-sensitive neurons in adult mouse DRG that can be excited by NGF is more sensitive to CAPS, responds with stronger signals and is further sensitised by transient exposure to the neurotrophin.
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HÖGBACK, Susanna, Petra LEPPIMÄKI, Britt RUDNÄS, Sonja BJÖRKLUND, J. Peter SLOTTE, and Kid TÖRNQUIST. "Ceramide 1-phosphate increases intracellular free calcium concentrations in thyroid FRTL-5 cells: evidence for an effect mediated by inositol 1,4,5-trisphosphate and intracellular sphingosine 1-phosphate." Biochemical Journal 370, no. 1 (2003): 111–19. http://dx.doi.org/10.1042/bj20020970.
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Sphingolipid (SP) derivatives have diverse effects on the regulation of intracellular free calcium concentrations ([Ca2+]i) in a multitude of non-excitable cells. In the present investigation, the effect of C2-ceramide 1-phosphate (C1P) on [Ca2+]i was investigated in thyroid FRTL-5 cells. C1P evoked a concentration-dependent increase in [Ca2+]i, both in a calcium-containing and a calcium-free buffer. A substantial part of the C1P-evoked increase in [Ca2+]i was due to calcium entry. The effect of C1P was attenuated by overnight pretreatment of the cells with pertussis toxin. Similar results were obtained with C8-ceramide 1-phosphate, although the magnitude of the responses was smaller than with C1P. The phospholipase C inhibitor U73122 attenuated the effect of C1P. C1P invoked a small, but significant, increase in inositol 1,4,5-trisphosphate (IP3). However, the effect of C1P on [Ca2+]i was inhibited by neither Xestospongin C, 2-aminoethoxydiphenylborate nor neomycin. C1P mobilized calcium from an IP3-sensitive calcium store, as C1P did not increase [Ca2+]i in cells pretreated with thapsigargin. The effect of C1P on [Ca2+]i was potently attenuated by dihydrosphingosine and dimethylsphingosine, two inhibitors of sphingosine kinase, but not by the inactive SP-derivative N-acetyl sphingosine. Stimulating the cells with C1P evoked an increase in the production of intracellular sphingosine 1-phosphate. C1P did not modulate DNA synthesis or the forskolin-evoked production of cAMP. The results indicate that C1P may be an important SP participating in cellular signalling.
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Ambudkar, I. S. "Regulation of Calcium in Salivary Gland Secretion." Critical Reviews in Oral Biology & Medicine 11, no. 1 (2000): 4–25. http://dx.doi.org/10.1177/10454411000110010301.
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Neurotransmitter-regulation of fluid secretion in the salivary glands is achieved by a coordinated sequence of intracellular signaling events, including the activation of membrane receptors, generation of the intracellular second messenger, inositol 1,4,5, trisphosphate, internal Ca2+ release, and Ca2+ influx. The resulting increase in cytosolic [Ca2+ ] ([Ca2+]i) regulates a number of ion transporters, e.g., Ca2+-activated K+ channel, Na+/K+/2Cl - co-transporter in the basolateral membrane, and the Ca2+-activated Cl- channel in the luminal membrane, which are intricately involved in fluid secretion. Thus, regulation of [Ca2+]i is central to the regulation of salivary acinar cell function and is achieved by the concerted activities of several ion channels and Ca2+-pumps localized in various cellular membranes. Ca2+ pumps, present in the endoplasmic reticulum and the plasma membrane, serve to remove Ca2+ from the cytosol. Ca2+ channels present in the endoplasmic reticulum and the plasma membrane facilitate rapid influx of Ca2+ into the cytosol from the internal Ca2+ stores and from the external medium, respectively. It is well-established that prolonged fluid secretion is regulated via a sustained elevation in [Ca2+]i that is primarily achieved by the influx of Ca2+ into the cell from the external medium. This Ca2+ influx occurs via a putative plasma-membrane-store-operated Ca2+ channel which has not yet been identified in any non-excitable cell type. Understanding the molecular nature of this Ca2+ influx mechanism is critical to our understanding of Ca2+ signaling in salivary gland cells. This review focuses on the various active and passive Ca 2+ transport mechanisms in salivary gland cells-their localization, regulation, and role in neurotransmitter-regulation of fluid secretion. In addition to a historical perspective of Ca2+ signaling, recent findings and challenging problems facing this field are highlighted.
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Reiser, G., F. Donie, and F. J. Binmoller. "Serotonin regulates cytosolic Ca2+ activity and membrane potential in a neuronal and in a glial cell line via 5-HT3 and 5-HT2 receptors by different mechanisms." Journal of Cell Science 93, no. 3 (1989): 545–55. http://dx.doi.org/10.1242/jcs.93.3.545.
Full textAbstract:
The mechanisms of action of two different serotonin receptors, found in a neuronal cell line (neuroblastoma X glioma hybrid cells) and in a non-excitable glioma cell line, were explored. In both cell lines, serotonin induced a dose-dependent, transient rise of cytosolic Ca2+ activity (measured by fura-2 or indo-1 fluorescence). Ca2+ channel blockers (Ni2+ and La3+, not nifedipine) suppressed the Ca2+ response to serotonin in the hybrid cells but not in the glioma cells. After application of Ca2+ ionophores (ionomycin and A23187) in order to short-circuit internal Ca2+ stores, serotonin was still able to induce a Ca2+ response in the hybrid cells but not in the glioma cells. Serotonin dose-dependently stimulated the rate of 45Ca2+ uptake several-fold in the hybrid cells, but hardly at all in the glioma cells. Thus, in the neuronal cell line cytosolic Ca2+ activity is raised through enhancement of Ca2+ entry into the cells from the extracellular environment via 5-HT3 receptors (blocked by ICS 205–930, MDL 72222 and GR 38032 F). The depolarization response caused by serotonin in the hybrid cells is due to activation of cation conductance(s), obviously allowing entry of extracellular Ca2+. In contrast to the neuronal cell line, in the glial cell line the rise of Ca2+ activity is mediated by ketanserin-susceptible 5-HT2 receptors (not affected by treatment with pertussis toxin) mainly liberating Ca2+ from internal stores. In the glioma cells the release of Ca2+ from internal stores leads to opening of Ca2+-dependent K+ channels, responsible for the hyperpolarizing response. Thus, the neuronal and the glial cell lines might provide suitable systems in which to study the diverse cellular functions triggered by the rise of cytosolic Ca2+ activity, which is caused by different serotonin receptors.
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McCarron, John G., John W. Craig, Karen N. Bradley, and Thomas C. Muir. "Agonist-induced phasic and tonic responses in smooth muscle are mediated by InsP3." Journal of Cell Science 115, no. 10 (2002): 2207–18. http://dx.doi.org/10.1242/jcs.115.10.2207.
Full textAbstract:
Many cellular functions are regulated by agonist-induced InsP3-evoked Ca2+ release from the internal store. In non-excitable cells, predominantly, the initial Ca2+release from the store by InsP3 is followed by a more sustained elevation in [Ca2+]i via store-operated Ca2+ channels as a consequence of depletion of the store. Here, in smooth muscle, we report that the initial transient increase in Ca2+, from the internal store, is followed by a sustained response also as a consequence of depletion of the store (by InsP3), but, influx occurs via voltage-dependent Ca2+ channels. Contractions were measured in pieces of whole distal colon and membrane currents and [Ca2+]i in single colonic myocytes. Carbachol evoked phasic and tonic contractions; only the latter were abolished in Ca2+-free solution. The tonic component was blocked by the voltage-dependent Ca2+ channel blocker nimodipine but not by the store-operated channel blocker SKF 96365. InsP3 receptor inhibition, with 2-APB, attenuated both the phasic and tonic components. InsP3 may regulate tonic contractions via sarcolemma Ca2+ entry. In single cells,depolarisation (to ∼-20 mV) elevated [Ca2+]i and activated spontaneous transient outward currents (STOCs). CCh suppressed STOCs, as did caffeine and InsP3. InsP3 receptor blockade by 2-APB or heparin prevented CCh suppression of STOCs; protein kinase inhibition by H-7 or PKC19-36did not. InsP3 suppressed STOCs by depleting a Ca2+ store accessed separately by the ryanodine receptor (RyR). Thus depletion of the store by RyR activators abolished the InsP3-evoked Ca2+ transient. RyR inhibition (by tetracaine) reduced only STOCs but not the InsP3transient. InsP3 contributes to both phasic and tonic contractions. In the former, muscarinic receptor-evoked InsP3 releases Ca2+ from an internal store accessed by both InsP3 and RyR. Depletion of this store by InsP3 alone suppresses STOCs, depolarises the sarcolemma and permits entry of Ca2+ to generate the tonic component. Therefore, by lowering the internal store Ca2+ content,InsP3 may generate a sustained smooth muscle contraction. These results provide a mechanism to account for phasic and tonic smooth muscle contraction following receptor activation.
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Pillozzi, Serena, Marika Masselli, Marinella Veltroni, et al. "Role of the Ether-a-gò-gò-Related Gene 1B Isoform in Hematopoiesis." Blood 120, no. 21 (2012): 1222. http://dx.doi.org/10.1182/blood.v120.21.1222.1222.
Full textAbstract:
Abstract Abstract 1222 Normal hematopoiesis is characterized by the tuned regulation of self renewal, proliferation, differentiation and migration of hematopoietic stem cells and HSC-derived multipotent and lineage-committed hemopoietic progenitor cells. This regulation is a complex process, which requires several levels of control provided by the activity of numerous membrane receptors and soluble proteins, which mediate the communication among hematopoietic cells, and between the cells and the microenvironment. In this contest, ion channels must be mentioned. Indeed, besides their canonical role in cell excitability, they can also modulate different cellular functions, such as proliferation, apoptosis and differentiation, in both excitable and non excitable cells. This role is also relevant in hematopoietic cells, where ion channels have a clear role in different functions of fully differentiated cells (Int Rev Cell Mol Biol. 2010;279:135–190). On these bases, we analyzed the role of ether a gò-gò-related gene 1 (ERG1) channels in normal hematopoiesis. In particular, we performed lack of function studies using a murine ERG1 knock out (KO) model (in SV129 strain). Since mice with a general and complete KO of the whole ERG1 gene die during early development, we analyzed mice with a selective deletion of the ERG1B isoform (ERG1B−/− mice, Mol Cell Biol. 1003;23(6):1856–1862), which is the ERG1 isoform mostly expressed in leukemic blasts (Blood. 2007;110(4):1238–1250). Such mice are viable and do not show any life threatening physical or behavioral abnormalities. First, we verified ERG1 transcripts expression in wild type SV129 mice (WT): both transcripts were expressed in spleen and thymus with higher values for the ERG1A isoform; ERG1B isoform presented a good expression level in bone marrow (BM) especially in the Sca-1+ population. Consequently we performed experiments to evaluate the role of ERG1B in normal hematopoiesis. Young (0–3 months old) KO mice presented a reduced number of CFUs (colony forming units) in the BM. CFUs levels were restored in adult mice. BM of KO mice showed hypocellularity and an increased number of megakaryocytes intriguingly associated with a reduction of erythrocytes (Ter119+). As evidenced by the histological analysis, splenomegaly of KO mice could be traced back to a great amount of mature red blood cells, filling the interfollicular space of the red pulp and subcapsulary space. Such splenic congestion in ERG1B−/− mice is accompanied by a relative decrease in the number of megakaryocytes, as well as by a reduced capacity to develop CFUs. On the whole, these data are suggestive of a failure of spleen hemopoiesis, with a concomitant red cell engulfment that lead to a putative erythropoiesis that occurs locally in the spleen maybe due to reprogrammation of hematopoietic cells of different lineage. To better characterize hematopoiesis in ERG1B−/− mouse model we performed two different stress tests: myelotoxicity and acute hemolytic anemia induction. Myelotoxicity was induced by single dose injection of cyclophosphamide (450 mg/Kg) in both WT and KO mice. From this induction we expected a decreased myelopoiesis, mostly affecting granulocytes and monocytes, followed by a rebound due to the capacity of the mice to undertake myelopoiesis. In KO model this compensation was absent suggesting a functional defect into the myeloid lineage correlated with ERG1B deletion. Finally, we induced acute anemia in mice testing their response to phenylhydrazine (PHZ, 60 mg/Kg). As expected, in WT mice, RBCs value rapidly declined followed by a compensatory erythropoiesis. In ERG1B−/− mice, we observed a reduced capacity to recover physiological RBCs values. Such results suggest that a functional defect occurred also into the erythroid lineage. On the whole, the present study provides evidence that the ERG1B isoform exerts a relevant role in hematopoiesis, driving the commitment and maturation of different hematopoietic cell populations. Disclosures: No relevant conflicts of interest to declare.
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Banrezes, B., S. Toth, D. Huneau, R. Schultz, and J. P. Ozil. "297A METHOD TO DRIVE CALCIUM SIGNALLING DYNAMICS IN FERTILIZED MOUSE EGGS." Reproduction, Fertility and Development 16, no. 2 (2004): 268. http://dx.doi.org/10.1071/rdv16n1ab297.
Full textAbstract:
Following fertilization, eggs exhibit a series of repetitive increases in intracellular calcium that activate development. The developmental impact of the long-lasting series of Ca2+ signals is still a subject of controversy. Although several studies using parthenogenetically activated eggs suggest that Ca2+ dynamics affect post-implantation development, artificial stimulation of Ca2+ signaling after ICSI in bovine eggs shows that development still remains poor in comparison to fertilized eggs. Such divergence between parthenogenetic studies and those aimed at stimulating ICSI eggs makes it impossible to draw any conclusions regarding the function of Ca2+ signaling for two reasons. First, non-fertilized eggs do not release Ca2+ from intracellular stores and their development is compromised due to the absence of paternally-derived chromosomes. Second, because ICSI eggs are excitable, Ca2+ stimulation generates additional Ca2+ oscillations that might compromise their development. Moreover, in both cases, Ca2+ signaling is not physiological. To understand better the function of Ca2+ signaling at fertilization, we developed a new approach based on micro fluidic technology that makes it possible to drive Ca2+ signal dynamics of fertilized eggs with no apparent deleterious effects. This method relies on the fact that the properties of the IP3 receptor (IP3R) calcium channel are changed after fertilization, and IP3 and Ca2+ act as co-agonists to cause Ca2+-induced Ca2+ release (CICR) from intracellular stores. Because Ca2+ has both an inhibiting and a stimulating function, we exploited these opposing properties. First, we inhibited Ca2+ release by external washing with Ca2+-free medium;; this extra cellular washing decreases cytosolic [Ca2+]I, and facilitates dissociation of Ca2+ ions from the IP3R that in turn decreases the probability of IP3R channel opening. Second, once the IP3R is inhibited, a simple injection of Ca2+ ions by electropermeabilization triggers channel opening and induces Ca2+ release. Then, by just varying the time interval and the number of the electrical pulses, it is possible to drive the dynamics of the CICR process that initiates development. Intracellular Ca2+ imaging demonstrated that fertilized eggs subjected to 24 electrical pulses (1.45kVcm−1) every 8min for 3h in the microfluidic processor responded by exhibiting 24 induced-Ca2+ transients that are caused by calcium release from intracellular stores. All auto-regenerative responses between pulses were inhibited. Among 60 treated embryos transferred to pseudo-pregnant recipients, 40 (67%) developed to term, with birth of live offspring, thus demonstrating that this new methodology does not compromise development. Because the eggs are fertilized, it now becomes possible to study the function of Ca2+ signaling during egg activation and to evaluate its developmental impact, if any, in association with genomic approaches.
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KESSEBÖHMER, M., J. D. M. RADEMACHER, and D. ULBRICH. "Dynamics and topological entropy of 1D Greenberg–Hastings cellular automata." Ergodic Theory and Dynamical Systems, March 9, 2020, 1–34. http://dx.doi.org/10.1017/etds.2020.18.
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In this paper we analyse the non-wandering set of one-dimensional Greenberg–Hastings cellular automaton models for excitable media with $e\geqslant 1$ excited and $r\geqslant 1$ refractory states and determine its (strictly positive) topological entropy. We show that it results from a Devaney chaotic closed invariant subset of the non-wandering set that consists of colliding and annihilating travelling waves, which is conjugate to a skew-product dynamical system of coupled shift dynamics. Moreover, we determine the remaining part of the non-wandering set explicitly as a Markov system with strictly less topological entropy that also scales differently for large $e,r$ .
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Lazzari-Dean, Julia R., Anneliese MM Gest, and Evan W. Miller. "Optical estimation of absolute membrane potential using fluorescence lifetime imaging." eLife 8 (September 23, 2019). http://dx.doi.org/10.7554/elife.44522.
Full textAbstract:
All cells maintain ionic gradients across their plasma membranes, producing transmembrane potentials (Vmem). Mounting evidence suggests a relationship between resting Vmem and the physiology of non-excitable cells with implications in diverse areas, including cancer, cellular differentiation, and body patterning. A lack of non-invasive methods to record absolute Vmem limits our understanding of this fundamental signal. To address this need, we developed a fluorescence lifetime-based approach (VF-FLIM) to visualize and optically quantify Vmem with single-cell resolution in mammalian cell culture. Using VF-FLIM, we report Vmem distributions over thousands of cells, a 100-fold improvement relative to electrophysiological approaches. In human carcinoma cells, we visualize the voltage response to growth factor stimulation, stably recording a 10–15 mV hyperpolarization over minutes. Using pharmacological inhibitors, we identify the source of the hyperpolarization as the Ca2+-activated K+ channel KCa3.1. The ability to optically quantify absolute Vmem with cellular resolution will allow a re-examination of its signaling roles.
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Zhang, Isis, and Huijuan Hu. "Store-Operated Calcium Channels in Physiological and Pathological States of the Nervous System." Frontiers in Cellular Neuroscience 14 (November 26, 2020). http://dx.doi.org/10.3389/fncel.2020.600758.
Full textAbstract:
Store-operated calcium channels (SOCs) are widely expressed in excitatory and non-excitatory cells where they mediate significant store-operated calcium entry (SOCE), an important pathway for calcium signaling throughout the body. While the activity of SOCs has been well studied in non-excitable cells, attention has turned to their role in neurons and glia in recent years. In particular, the role of SOCs in the nervous system has been extensively investigated, with links to their dysregulation found in a wide variety of neurological diseases from Alzheimer’s disease (AD) to pain. In this review, we provide an overview of their molecular components, expression, and physiological role in the nervous system and describe how the dysregulation of those roles could potentially lead to various neurological disorders. Although further studies are still needed to understand how SOCs are activated under physiological conditions and how they are linked to pathological states, growing evidence indicates that SOCs are important players in neurological disorders and could be potential new targets for therapies. While the role of SOCE in the nervous system continues to be multifaceted and controversial, the study of SOCs provides a potentially fruitful avenue into better understanding the nervous system and its pathologies.