Cell calcium最新文献

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Corrigendum to “Modulating TRPV4 channels with paclitaxel and lithium” [Cell Calcium 91 (2020) 102266] “用紫杉醇和锂调制TRPV4通道”的勘误表[Cell Calcium 91(2020) 102266]。
IF 4.3 2区 生物学
Cell calcium Pub Date : 2025-01-01 DOI: 10.1016/j.ceca.2024.102988
Julio C. Sánchez , Laura V. Muñoz , Barbara E. Ehrlich
{"title":"Corrigendum to “Modulating TRPV4 channels with paclitaxel and lithium” [Cell Calcium 91 (2020) 102266]","authors":"Julio C. Sánchez , Laura V. Muñoz , Barbara E. Ehrlich","doi":"10.1016/j.ceca.2024.102988","DOIUrl":"10.1016/j.ceca.2024.102988","url":null,"abstract":"","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"125 ","pages":"Article 102988"},"PeriodicalIF":4.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142920904","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}
引用次数: 0
Regulation of SR and mitochondrial Ca2+ signaling by L-type Ca2+ channels and Na/Ca exchanger in hiPSC–CMs l型Ca2+通道和Na/Ca交换器对hiPSC-CMs中SR和线粒体Ca2+信号的调控
IF 4.3 2区 生物学
Cell calcium Pub Date : 2025-01-01 DOI: 10.1016/j.ceca.2024.102985
Xiao-Hua Zhang, Martin Morad
{"title":"Regulation of SR and mitochondrial Ca2+ signaling by L-type Ca2+ channels and Na/Ca exchanger in hiPSC–CMs","authors":"Xiao-Hua Zhang,&nbsp;Martin Morad","doi":"10.1016/j.ceca.2024.102985","DOIUrl":"10.1016/j.ceca.2024.102985","url":null,"abstract":"<div><h3>Rationale &amp; methods</h3><div>While signaling of cardiac SR by surface membrane proteins (I<sub>Ca</sub> &amp; I<sub>NCX</sub>) is well studied, the regulation of mitochondrial Ca<sup>2+</sup> by plasmalemmal proteins remains less explored. Here we have examined the signaling of mitochondria and SR by surface-membrane calcium-transporting proteins, using genetically engineered targeted fluorescent probes, mito-GCamP6 and R-CEPIA1er.</div></div><div><h3>Results</h3><div>In voltage-clamped and TIRF-imaged cardiomyocytes, low Na<sup>+</sup> induced SR Ca<sup>2+</sup> release was suppressed by short pre-exposures to ∼100 nM FCCP, suggesting mitochondrial Ca<sup>2+</sup> contribution to low Na<sup>+</sup> triggered SR Ca<sup>2+</sup>release. Even though low Na<sup>+</sup>- or caffeine-triggered SR Ca<sup>2+</sup> release activated <em><u>global</u></em> mitochondrial Ca<sup>2+</sup> uptake, <u>f</u><em><u>ocal</u></em> mitochondrial Ca<sup>2+</sup> signals varied in kinetics and magnitude, showing uptake or release of calcium, depending on cellular location of mitochondria. In spontaneously pacing cells, sustained caffeine exposures depleted the SR Ca<sup>2+</sup> content activating mitochondrial Ca<sup>2+</sup> uptake followed by sustained mitochondrial pacing. Spontaneous hiPSC<img>CMs pacing was strongly suppressed by L-type calcium channels blockers, but not by inhibiting SERCA2a by CPA.</div></div><div><h3>Conclusion</h3><div>Spontaneous hiPSC<img>CMs pacing is triggered by influx of calcium through L-type Ca<sup>2+</sup> channel that gates the release of SR pools supplemented by NCX-mediated mitochondrial calcium contribution.</div></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"125 ","pages":"Article 102985"},"PeriodicalIF":4.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142853112","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}
引用次数: 0
Roles for TRPV4 in disease: A discussion of possible mechanisms TRPV4在疾病中的作用:可能机制的讨论。
IF 4.3 2区 生物学
Cell calcium Pub Date : 2024-12-01 DOI: 10.1016/j.ceca.2024.102972
Ana M. Hernández-Vega , Refugio García-Villegas , Tamara Rosenbaum
{"title":"Roles for TRPV4 in disease: A discussion of possible mechanisms","authors":"Ana M. Hernández-Vega ,&nbsp;Refugio García-Villegas ,&nbsp;Tamara Rosenbaum","doi":"10.1016/j.ceca.2024.102972","DOIUrl":"10.1016/j.ceca.2024.102972","url":null,"abstract":"<div><div>The transient receptor potential vanilloid 4 (TRPV4) ion channel is a ubiquitously expressed Ca<sup>2+</sup>-permeable ion channel that controls intracellular calcium ([Ca<sup>2+</sup>]<sub>i</sub>) homeostasis in various types of cells. The physiological roles for TRPV4 are tissue specific and the mechanisms behind this specificity remain mostly unclarified. It is noteworthy that mutations in the TRPV4 channel have been associated to a broad spectrum of congenital diseases, with most of these mutations mainly resulting in gain-of-function. Mutations have been identified in human patients showing a variety of phenotypes and symptoms, mostly related to skeletal and neuromuscular disorders. Since TRPV4 is so widely expressed throughout the body, it comes as no surprise that the literature is growing in evidence linking this protein to malfunction in systems other than the skeletal and neuromuscular. In this review, we summarize the expression patterns of TRPV4 in several tissues and highlight findings of recent studies that address critical structural and functional features of this channel, particularly focusing on its interactions and signaling pathways related to Ca<sup>2+</sup> entry. Moreover, we discuss the roles of TRPV4 mutations in some diseases and pinpoint some of the mechanisms underlying pathological states where TRPV4’s malfunction is prominent.</div></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"124 ","pages":"Article 102972"},"PeriodicalIF":4.3,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142749679","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}
引用次数: 0
PIP2 primes IP3 receptor activity: It takes at least three IP3s to open! PIP2 激发了 IP3 受体的活性:至少需要三个 IP3 才能打开!
IF 4.3 2区 生物学
Cell calcium Pub Date : 2024-11-20 DOI: 10.1016/j.ceca.2024.102970
Vikas Arige, David I. Yule
{"title":"PIP2 primes IP3 receptor activity: It takes at least three IP3s to open!","authors":"Vikas Arige,&nbsp;David I. Yule","doi":"10.1016/j.ceca.2024.102970","DOIUrl":"10.1016/j.ceca.2024.102970","url":null,"abstract":"","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"124 ","pages":"Article 102970"},"PeriodicalIF":4.3,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142721672","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}
引用次数: 0
NAADP signaling: Master manipulation NAADP 信号:主控操作
IF 4.3 2区 生物学
Cell calcium Pub Date : 2024-11-17 DOI: 10.1016/j.ceca.2024.102969
Qianru Mu , Jade L. Harris , David I. Yule , James T. Slama , Jonathan S. Marchant , Sandip Patel
{"title":"NAADP signaling: Master manipulation","authors":"Qianru Mu ,&nbsp;Jade L. Harris ,&nbsp;David I. Yule ,&nbsp;James T. Slama ,&nbsp;Jonathan S. Marchant ,&nbsp;Sandip Patel","doi":"10.1016/j.ceca.2024.102969","DOIUrl":"10.1016/j.ceca.2024.102969","url":null,"abstract":"","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"124 ","pages":"Article 102969"},"PeriodicalIF":4.3,"publicationDate":"2024-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142695392","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}
引用次数: 0
Electrogenic and non-electrogenic ion antiporters participate in controling membrane potential 电性和非电性离子反转运体参与控制膜电位。
IF 4.3 2区 生物学
Cell calcium Pub Date : 2024-11-16 DOI: 10.1016/j.ceca.2024.102971
Pablo Hernansanz-Agustín , Carmen Morales-Vidal , Enrique Calvo , Paolo Natale , Yolanda Martí-Mateos , Sara Natalia Jaroszewicz , José Luis Cabrera-Alarcón , Rebeca Acín-Pérez , Iván López-Montero , Jesús Vázquez , José Antonio Enríquez
{"title":"Electrogenic and non-electrogenic ion antiporters participate in controling membrane potential","authors":"Pablo Hernansanz-Agustín ,&nbsp;Carmen Morales-Vidal ,&nbsp;Enrique Calvo ,&nbsp;Paolo Natale ,&nbsp;Yolanda Martí-Mateos ,&nbsp;Sara Natalia Jaroszewicz ,&nbsp;José Luis Cabrera-Alarcón ,&nbsp;Rebeca Acín-Pérez ,&nbsp;Iván López-Montero ,&nbsp;Jesús Vázquez ,&nbsp;José Antonio Enríquez","doi":"10.1016/j.ceca.2024.102971","DOIUrl":"10.1016/j.ceca.2024.102971","url":null,"abstract":"<div><div>In a comment to our recent publication, Nicholls question our results and interpretation based on theoretical arguments that reveal a profound misunderstanding of our publication.</div></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"124 ","pages":"Article 102971"},"PeriodicalIF":4.3,"publicationDate":"2024-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142692782","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}
引用次数: 0
Commentary on: Li et al.; Ca2+ transients on the T cell surface trigger rapid integrin activation in a timescale of seconds. Nature Communications (2024) 评论Li等人; T细胞表面的Ca2+瞬态可在数秒内触发整合素的快速激活。自然-通讯》(2024 年)。
IF 4.3 2区 生物学
Cell calcium Pub Date : 2024-11-09 DOI: 10.1016/j.ceca.2024.102968
Mohan Manjegowda, Bimal N. Desai
{"title":"Commentary on: Li et al.; Ca2+ transients on the T cell surface trigger rapid integrin activation in a timescale of seconds. Nature Communications (2024)","authors":"Mohan Manjegowda,&nbsp;Bimal N. Desai","doi":"10.1016/j.ceca.2024.102968","DOIUrl":"10.1016/j.ceca.2024.102968","url":null,"abstract":"","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"124 ","pages":"Article 102968"},"PeriodicalIF":4.3,"publicationDate":"2024-11-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142643740","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}
引用次数: 0
Distribution and calcium signaling function of somatostatin receptor subtypes in rat pituitary 大鼠垂体中体生长抑素受体亚型的分布和钙信号功能
IF 4.3 2区 生物学
Cell calcium Pub Date : 2024-11-02 DOI: 10.1016/j.ceca.2024.102967
Sonja Sivcev , Stephanie Constantin , Kosara Smiljanic , Srdjan J. Sokanovic , Patrick A. Fletcher , Arthur S. Sherman , Hana Zemkova , Stanko S. Stojilkovic
{"title":"Distribution and calcium signaling function of somatostatin receptor subtypes in rat pituitary","authors":"Sonja Sivcev ,&nbsp;Stephanie Constantin ,&nbsp;Kosara Smiljanic ,&nbsp;Srdjan J. Sokanovic ,&nbsp;Patrick A. Fletcher ,&nbsp;Arthur S. Sherman ,&nbsp;Hana Zemkova ,&nbsp;Stanko S. Stojilkovic","doi":"10.1016/j.ceca.2024.102967","DOIUrl":"10.1016/j.ceca.2024.102967","url":null,"abstract":"<div><div>The somatostatin (SST) receptor family controls pituitary hormone secretion, but the distribution and specific roles of these receptors on the excitability and voltage-gated calcium signaling of hormone producing pituitary cells have not been fully characterized. Here we show that the rat pituitary gland expressed <em>Sstr1, Sstr2, Sstr3,</em> and <em>Sstr5</em> receptor genes in a cell type-specific manner: <em>Sstr1</em> and <em>Sstr2</em> in thyrotrophs, <em>Sstr3</em> in gonadotrophs and lactotrophs, <em>Sstr2, Sstr3</em>, and <em>Sstr5</em> in somatotrophs, and none in corticotrophs and melanotrophs. Most gonadotrophs and thyrotrophs spontaneously fired high-amplitude single action potentials, which were silenced by SST without affecting intracellular calcium concentrations. In contrast, lactotrophs and somatotrophs spontaneously fired low-amplitude plateau-bursting action potentials in conjunction with calcium transients, both of which were silenced by SST. Moreover, SST inhibited GPCR-induced voltage-gated calcium signaling and hormone secretion in all cell types expressing SST receptors, but the inhibition was more pronounced in somatotrophs. The pattern of inhibition of electrical activity and calcium signaling was consistent with both direct and indirect inhibition of voltage-gated calcium channels, the latter being driven by cell type-specific hyperpolarization. These results indicate that the action of SST in somatotrophs is enhanced by the expression of several types of SST receptors and their slow desensitization, that SST may play a role in the electrical resynchronization of gonadotrophs, thyrotrophs, and lactotrophs, and that the lack of SST receptors in corticotrophs and melanotrophs keeps them excitable and ready to responses to stress.</div></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"124 ","pages":"Article 102967"},"PeriodicalIF":4.3,"publicationDate":"2024-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142614266","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}
引用次数: 0
Calcium signals as regulators of ferroptosis in cancer 钙信号是癌症中铁蛋白沉积的调节因子
IF 4.3 2区 生物学
Cell calcium Pub Date : 2024-10-29 DOI: 10.1016/j.ceca.2024.102966
Ioana Stejerean-Todoran , Christine S. Gibhardt , Ivan Bogeski
{"title":"Calcium signals as regulators of ferroptosis in cancer","authors":"Ioana Stejerean-Todoran ,&nbsp;Christine S. Gibhardt ,&nbsp;Ivan Bogeski","doi":"10.1016/j.ceca.2024.102966","DOIUrl":"10.1016/j.ceca.2024.102966","url":null,"abstract":"<div><div>The field of ferroptosis research has grown exponentially since this form of cell death was first identified over a decade ago. Ferroptosis, an iron- and ROS-dependent type of cell death, is controlled by various metabolic pathways, including but not limited to redox and calcium (Ca<sup>2+</sup>) homeostasis, iron fluxes, mitochondrial function and lipid metabolism. Importantly, therapy-resistant tumors are particularly susceptible to ferroptotic cell death, rendering ferroptosis a promising therapeutic strategy against numerous malignancies. Calcium signals are important regulators of both cancer progression and cell death, with recent studies indicating their involvement in ferroptosis. Cells undergoing ferroptosis are characterized by plasma membrane rupture and the formation of nanopores, which facilitate influx of ions such as Ca<sup>2+</sup> into the affected cells. Furthermore, mitochondrial Ca²⁺ levels have been implicated in directly influencing the cellular response to ferroptosis. Despite the remarkable progress made in the field, our understanding of the contribution of Ca<sup>2+</sup> signals to ferroptosis remains limited. Here, we summarize key connections between Ca²⁺ signaling and ferroptosis in cancer pathobiology and discuss their potential therapeutic significance.</div></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"124 ","pages":"Article 102966"},"PeriodicalIF":4.3,"publicationDate":"2024-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142586318","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}
引用次数: 0
GPCR signalling: Yet another variant route in a highly complex road map GPCR 信号:高度复杂路线图中的另一条变异路线
IF 4.3 2区 生物学
Cell calcium Pub Date : 2024-10-24 DOI: 10.1016/j.ceca.2024.102965
Alexander Demby, Manuela Zaccolo
{"title":"GPCR signalling: Yet another variant route in a highly complex road map","authors":"Alexander Demby,&nbsp;Manuela Zaccolo","doi":"10.1016/j.ceca.2024.102965","DOIUrl":"10.1016/j.ceca.2024.102965","url":null,"abstract":"","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"124 ","pages":"Article 102965"},"PeriodicalIF":4.3,"publicationDate":"2024-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142552072","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}
引用次数: 0
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