Cell calcium最新文献

{"title":"TRPV1: Receptor structure, activation, modulation and role in neuro-immune interactions and pain","authors":"Thaila Kawane Euflazio Maximiano ,&nbsp;Jessica Aparecida Carneiro ,&nbsp;Victor Fattori ,&nbsp;Waldiceu A. Verri","doi":"10.1016/j.ceca.2024.102870","DOIUrl":"10.1016/j.ceca.2024.102870","url":null,"abstract":"<div><p>In the 1990s, the identification of a non-selective ion channel, especially responsive to capsaicin, revolutionized the studies of somatosensation and pain that were to follow. The TRPV1 channel is expressed mainly in neuronal cells, more specifically, in sensory neurons responsible for the perception of noxious stimuli. However, its presence has also been detected in other non-neuronal cells, such as immune cells, β- pancreatic cells, muscle cells and adipocytes. Activation of the channel occurs in response to a wide range of stimuli, such as noxious heat, low pH, gasses, toxins, endocannabinoids, lipid-derived endovanilloid, and chemical agents, such as capsaicin and resiniferatoxin. This activation results in an influx of cations through the channel pore, especially calcium. Intracellular calcium triggers different responses in sensory neurons. Dephosphorylation of the TRPV1 channel leads to its desensitization, which disrupts its function, while its phosphorylation increases the channel's sensitization and contributes to the channel's rehabilitation after desensitization. Kinases, phosphoinositides, and calmodulin are the main signaling pathways responsible for the channel's regulation. Thus, in this review we provide an overview of TRPV1 discovery, its tissue expression as well as on the mechanisms by which TRPV1 activation (directly or indirectly) induces pain in different disease models.</p></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"119 ","pages":"Article 102870"},"PeriodicalIF":4.0,"publicationDate":"2024-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140076075","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neighbourhood Watch: Two-pore-2 channels talking to IP3 receptors","authors":"David N Criddle,&nbsp;Alexei V Tepikin","doi":"10.1016/j.ceca.2024.102868","DOIUrl":"https://doi.org/10.1016/j.ceca.2024.102868","url":null,"abstract":"<div><p>The recent elegant study by Y. Yuan and colleagues examined functional relationships between the lysosomal two-pore channels 2 (TPC2) and IP3 receptors (IP3Rs) located in the endoplasmic reticulum <span>[1]</span>. The findings of this study suggest functional coupling of these channels and receptors. The study also describes interesting novel phenomena, which may indicate an additional coupling mechanism.</p></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"119 ","pages":"Article 102868"},"PeriodicalIF":4.0,"publicationDate":"2024-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140062862","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recognition of granulocyte-macrophage colony-stimulating factor by specific S100 proteins","authors":"Alexey S. Kazakov ,&nbsp;Victoria A. Rastrygina ,&nbsp;Alisa A. Vologzhannikova ,&nbsp;Marina Y. Zemskova ,&nbsp;Lolita A. Bobrova ,&nbsp;Evgenia I. Deryusheva ,&nbsp;Maria E. Permyakova ,&nbsp;Andrey S. Sokolov ,&nbsp;Ekaterina A. Litus ,&nbsp;Marina P. Shevelyova ,&nbsp;Vladimir N. Uversky ,&nbsp;Eugene A. Permyakov ,&nbsp;Sergei E. Permyakov","doi":"10.1016/j.ceca.2024.102869","DOIUrl":"10.1016/j.ceca.2024.102869","url":null,"abstract":"<div><p>Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a pleiotropic myelopoietic growth factor and proinflammatory cytokine, clinically used for multiple indications and serving as a promising target for treatment of many disorders, including cancer, multiple sclerosis, rheumatoid arthritis, psoriasis, asthma, COVID-19. We have previously shown that dimeric Ca²⁺-bound forms of S100A6 and S100P proteins, members of the multifunctional S100 protein family, are specific to GM-CSF. To probe selectivity of these interactions, the affinity of recombinant human GM-CSF to dimeric Ca²⁺-loaded forms of 18 recombinant human S100 proteins was studied by surface plasmon resonance spectroscopy. Of them, only S100A4 protein specifically binds to GM-CSF with equilibrium dissociation constant, <em>K</em>_d, values of 0.3–2 μM, as confirmed by intrinsic fluorescence and chemical crosslinking data. Calcium removal prevents S100A4 binding to GM-CSF, whereas monomerization of S100A4/A6/P proteins disrupts S100A4/A6 interaction with GM-CSF and induces a slight decrease in S100P affinity for GM-CSF. Structural modelling indicates the presence in the GM-CSF molecule of a conserved S100A4/A6/P-binding site, consisting of the residues from its termini, helices I and III, some of which are involved in the interaction with GM-CSF receptors. The predicted involvement of the ‘hinge’ region and F89 residue of S100P in GM-CSF recognition was confirmed by mutagenesis. Examination of S100A4/A6/P ability to affect GM-CSF signaling showed that S100A4/A6 inhibit GM-CSF-induced suppression of viability of monocytic THP-1 cells. The ability of the S100 proteins to modulate GM-CSF activity is relevant to progression of various neoplasms and other diseases, according to bioinformatics analysis. The direct regulation of GM-CSF signaling by extracellular forms of the S100 proteins should be taken into account in the clinical use of GM-CSF and development of the therapeutic interventions targeting GM-CSF or its receptors.</p></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"119 ","pages":"Article 102869"},"PeriodicalIF":4.0,"publicationDate":"2024-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140076039","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “Mutations and clinical significance of calcium voltage-gated channel subunit alpha 1E (CACNA1E) in non-small cell lung cancer” [Cell Calcium 102 (2022) 102527]","authors":"SH Gao ,&nbsp;GZ Wang ,&nbsp;LP Wang ,&nbsp;L Feng ,&nbsp;YC Zhou ,&nbsp;XJ Yu ,&nbsp;F Liang ,&nbsp;FY Yang ,&nbsp;Z Wang ,&nbsp;BB Sun ,&nbsp;D Wang ,&nbsp;LJ Liang ,&nbsp;DW Xie ,&nbsp;S Zhao ,&nbsp;HP Feng ,&nbsp;X Li ,&nbsp;KK Li ,&nbsp;TS Tang ,&nbsp;YC Huang ,&nbsp;SQ Wang ,&nbsp;GB Zhou","doi":"10.1016/j.ceca.2024.102866","DOIUrl":"https://doi.org/10.1016/j.ceca.2024.102866","url":null,"abstract":"","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"119 ","pages":"Article 102866"},"PeriodicalIF":4.0,"publicationDate":"2024-02-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0143416024000241/pdfft?md5=c47ac62f359793f132f1fff0b81a0ea3&pid=1-s2.0-S0143416024000241-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139999790","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Newly uncovered Cryo-EM structures of mammalian NCXs set a new stage for resolving the underlying molecular mechanisms and drug discovery","authors":"Daniel Khananshvili","doi":"10.1016/j.ceca.2024.102867","DOIUrl":"https://doi.org/10.1016/j.ceca.2024.102867","url":null,"abstract":"<div><p>The membrane-abundant NCX proteins mediate an electrogenic ion exchange (3Na⁺:1Ca²⁺) in the Ca²⁺-exit or Ca²⁺-entry mode. The structurally related isoform/splice variants of NCX are expressed in a tissue-specific manner to shape Ca²⁺ signalling/homeostasis in diverse cell types. The lack of mammalian NCX structure hampered the functional and regulatory resolution of tissue-specific NCX variants and their pharmacological targeting. Recently unveiled Cryo-EM structures of human cardiac NCX1.1[1] and kidney NCX1.3[2] provide new opportunities for resolving structure/functional divergences among NCX variants and their pharmacological targeting.</p></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"119 ","pages":"Article 102867"},"PeriodicalIF":4.0,"publicationDate":"2024-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139993160","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NMDA receptor-mediated Ca2+ signaling: Impact on cell cycle regulation and the development of neurodegenerative diseases and cancer","authors":"Ana L. González-Cota ,&nbsp;Daniel Martínez-Flores ,&nbsp;Margarita Jacaranda Rosendo-Pineda ,&nbsp;Luis Vaca","doi":"10.1016/j.ceca.2024.102856","DOIUrl":"10.1016/j.ceca.2024.102856","url":null,"abstract":"<div><p>NMDA receptors are Ca²⁺-permeable ligand-gated ion channels that mediate fast excitatory transmission in the central nervous system. NMDA receptors regulate the proliferation and differentiation of neural progenitor cells and also play critical roles in neural plasticity, memory, and learning. In addition to their physiological role, NMDA receptors are also involved in glutamate-mediated excitotoxicity, which results from excessive glutamate stimulation, leading to Ca²⁺ overload, and ultimately to neuronal death. Thus, NMDA receptor-mediated excitotoxicity has been linked to several neurodegenerative diseases such as Alzheimer's, Parkinson's, Huntington's, dementia, and stroke. Interestingly, in addition to its effects on cell death, aberrant expression or activation of NMDA receptors is also involved in pathological cellular proliferation, and is implicated in the invasion and proliferation of various types of cancer. These disorders are thought to be related to the contribution of NMDA receptors to cell proliferation and cell death through cell cycle modulation. This review aims to discuss the evidence implicating NMDA receptor activity in cell cycle regulation and the link between aberrant NMDA receptor activity and the development of neurodegenerative diseases and cancer due to cell cycle dysregulation. The information presented here will provide insights into the signaling pathways and the contribution of NMDA receptors to these diseases, and suggests that NMDA receptors are promising targets for the prevention and treatment of these diseases, which are leading causes of death and disability worldwide.</p></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"119 ","pages":"Article 102856"},"PeriodicalIF":4.0,"publicationDate":"2024-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139874260","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SERCA-1 conformational change exerted by the Ca2+-channel blocker diltiazem affects mammalian skeletal muscle function","authors":"Aura Jiménez-Garduño ,&nbsp;Ibrahim Ramirez-Soto ,&nbsp;Ileana Miranda-Rodríguez ,&nbsp;Sofía Gitler ,&nbsp;Alicia Ortega","doi":"10.1016/j.ceca.2024.102852","DOIUrl":"10.1016/j.ceca.2024.102852","url":null,"abstract":"<div><p>In skeletal muscle (SM), inward Ca²⁺-currents have no apparent role in excitation-contraction coupling (e-c coupling), however the Ca²⁺-channel blocker can affect twitch and tetanic muscle in mammalian SM. Experiments were conducted to study how diltiazem (DLZ) facilitates e-c coupling and inhibits contraction. 1) In complete <em>Extensor Digitorum Longus</em> (EDL) muscle and single intact fibres, 0.03 mM DLZ causes twitch potentiation and decreases force during tetanic activity, with increased fatigue. 2) In split open fibres isolated from EDL fibres, DLZ inhibits sarcoplasmic reticulum (SR) Ca²⁺-loading in a dose-dependent manner and has a potentiating effect on caffeine-induced SR Ca²⁺-release. 3) In isolated light SR (LSR) vesicles, SERCA1 hydrolytic activity is not affected by DLZ up to 0.2 mM. However, ATP-dependent Ca²⁺-uptake was inhibited in a dose-dependent manner at a concentration where e-c coupling is changed. 4) The passive Ca²⁺-efflux from LSR was reduced by half with 0.03 mM diltiazem, indicating that SR leaking does not account for the decreased Ca²⁺-uptake. 5) The denaturation profile of the SERCA Ca²⁺-binding domain has lower thermal stability in the presence of DLZ in a concentration-dependent manner, having no effect on the nucleotide-binding domain. We conclude that the effect of DLZ on SM is exerted by crossing the sarcolemma and interacting directly with the SERCA Ca²⁺-binding domain, affecting SR Ca²⁺-loading during relaxation, which has a consequence on SM contractility. Diltiazem effect on SM could be utilized as a tool to understand SM e-c coupling and muscle fatigue.</p></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"119 ","pages":"Article 102852"},"PeriodicalIF":4.0,"publicationDate":"2024-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139823544","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Astrocytic chloride regulates brain function in health and disease","authors":"Verena Untiet","doi":"10.1016/j.ceca.2024.102855","DOIUrl":"https://doi.org/10.1016/j.ceca.2024.102855","url":null,"abstract":"<div><p>Chloride ions (Cl⁻) play a pivotal role in synaptic inhibition in the central nervous system, primarily mediated through ionotropic mechanisms. A recent breakthrough emphathizes the significant influence of astrocytic intracellular chloride concentration ([C<em>l</em>⁻]_i) regulation, a field still in its early stages of exploration. Typically, the [Cl⁻]_i in most animal cells is maintained at lower levels than the extracellular chloride [Cl⁻]_o, a critical balance to prevent cell swelling due to osmotic pressure. Various Cl⁻ transporters are expressed differently across cell types, fine-tuning the [Cl⁻]_i, while Cl⁻ gradients are utilised by several families of Cl⁻ channels. Although the passive distribution of ions within cells is governed by basic biophysical principles, astrocytes actively expend energy to sustain [Cl⁻]_i at much higher levels than those achieved passively, and much higher than neuronal [Cl⁻]_i. Beyond the role in volume regulation, astrocytic [Cl⁻]_i is dynamically linked to brain states and influences neuronal signalling in actively behaving animals. As a vital component of brain function, astrocytic [Cl⁻]_i also plays a role in the development of disorders where inhibitory transmission is disrupted. This review synthesises the latest insights into astrocytic [Cl⁻]_i, elucidating its role in modulating brain function and its implications in various pathophysiological conditions.</p></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"118 ","pages":"Article 102855"},"PeriodicalIF":4.0,"publicationDate":"2024-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0143416024000137/pdfft?md5=399770827cd04fe027a79eb81a968f1b&pid=1-s2.0-S0143416024000137-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139737445","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MLKL overexpression leads to Ca2+ and metabolic dyshomeostasis in a neuronal cell model","authors":"Sathyaseelan S Deepa ,&nbsp;Nidheesh Thadathil ,&nbsp;Jorge Corral ,&nbsp;Sabira Mohammed ,&nbsp;Sophia Pham ,&nbsp;Hadyn Rose ,&nbsp;Michael T Kinter ,&nbsp;Arlan Richardson ,&nbsp;Carlos Manlio Díaz-García","doi":"10.1016/j.ceca.2024.102854","DOIUrl":"10.1016/j.ceca.2024.102854","url":null,"abstract":"<div><p>The necroptotic effector molecule MLKL accumulates in neurons over the lifespan of mice, and its downregulation has the potential to improve cognition through neuroinflammation, and changes in the abundance of synaptic proteins and enzymes in the central nervous system. Notwithstanding, direct evidence of cell-autonomous effects of MLKL expression on neuronal physiology and metabolism are lacking. Here, we tested whether the overexpression of MLKL in the absence of cell death in the neuronal cell line Neuro-2a recapitulates some of the hallmarks of aging at the cellular level. Using genetically-encoded fluorescent biosensors, we monitored the cytosolic and mitochondrial Ca²⁺ levels, along with the cytosolic concentrations of several metabolites involved in energy metabolism (lactate, glucose, ATP) and oxidative stress (oxidized/reduced glutathione). We found that MLKL overexpression marginally decreased cell viability, however, it led to reduced cytosolic and mitochondrial Ca²⁺ elevations in response to Ca²⁺ influx from the extracellular space. On the contrary, Ca²⁺ signals were elevated after mobilizing Ca²⁺ from the endoplasmic reticulum. Transient elevations in cytosolic Ca²⁺, mimicking neuronal stimulation, lead to higher lactate levels and lower glucose concentrations in Neuro-2a cells when overexpressing MLKL, which suggest enhanced neuronal glycolysis. Despite these alterations, energy levels and glutathione redox state in the cell bodies remained largely preserved after inducing MLKL overexpression for 24–48 h. Taken together, our proof-of-concept experiments are consistent with the hypothesis that MLKL overexpression in the absence of cell death contributes to both Ca²⁺ and metabolic dyshomeostasis, which are cellular hallmarks of brain aging.</p></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"119 ","pages":"Article 102854"},"PeriodicalIF":4.0,"publicationDate":"2024-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139819369","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TRPV3 returns with a pleasant feeling of warmth","authors":"Michael Schaefer","doi":"10.1016/j.ceca.2024.102853","DOIUrl":"10.1016/j.ceca.2024.102853","url":null,"abstract":"","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"118 ","pages":"Article 102853"},"PeriodicalIF":4.0,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139667319","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}