Cell calciumPub Date : 2024-12-20DOI: 10.1016/j.ceca.2024.102987
Kriti Ahuja, Sharon Raju, Sakshi Dahiya, Rajender K Motiani
{"title":"ROS and calcium signaling are critical determinant of skin pigmentation.","authors":"Kriti Ahuja, Sharon Raju, Sakshi Dahiya, Rajender K Motiani","doi":"10.1016/j.ceca.2024.102987","DOIUrl":"https://doi.org/10.1016/j.ceca.2024.102987","url":null,"abstract":"<p><p>Pigmentation is a protective phenomenon that shields skin cells from UV-induced DNA damage. Perturbations in pigmentation pathways predispose to skin cancers and lead to pigmentary disorders. These ailments impart psychological trauma and severely affect the patients' quality of life. Emerging literature suggests that reactive oxygen species (ROS) and calcium (Ca<sup>2+</sup>) signaling modules regulate physiological pigmentation. Further, pigmentary disorders are associated with dysregulated ROS homeostasis and changes in Ca<sup>2+</sup> dynamics. Here, we systemically review the literature that demonstrates key role of ROS and Ca<sup>2+</sup> signaling in pigmentation and pigmentary disorders. Further, we discuss recent studies, which have revealed that organelle-specific Ca<sup>2+</sup> transport mechanisms are critical determinant of pigmentation. Importantly, we deliberate upon the possibility of clinical management of pigmentary disorders by therapeutically targeting ROS generation and cellular Ca<sup>2+</sup> handling toolkit. Finally, we highlight the key outstanding questions in the field that demand critical and timely attention. Although an important role of ROS and Ca<sup>2+</sup> signaling in regulating skin pigmentation has emerged, the underlying molecular mechanisms remain poorly understood. In future, it would be vital to investigate in detail the signaling cascades that connect perturbed ROS homeostasis and Ca<sup>2+</sup> signaling to human pigmentary disorders.</p>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"125 ","pages":"102987"},"PeriodicalIF":4.3,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142871458","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}
Cell calciumPub Date : 2024-12-13DOI: 10.1016/j.ceca.2024.102986
Leandro C Clementino, Andrew P Thomas, Emily M Rocha, Sabine Hilfiker
{"title":"A role for lysosomal calcium channels in mitigating mitochondrial damage and oxidative stress.","authors":"Leandro C Clementino, Andrew P Thomas, Emily M Rocha, Sabine Hilfiker","doi":"10.1016/j.ceca.2024.102986","DOIUrl":"https://doi.org/10.1016/j.ceca.2024.102986","url":null,"abstract":"<p><p>Elevated free fatty acids and oxidative stress may function as pathogenic factors in endothelial dysfunction that is associated with various cardiovascular complications. In recent work, Feng and colleagues report that activation of a lysosomal Ca<sup>2+</sup> channel may be a viable option to alleviate oxidative damage by boosting lysosome biogenesis and mitophagy.</p>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"125 ","pages":"102986"},"PeriodicalIF":4.3,"publicationDate":"2024-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142853110","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}
Cell calciumPub Date : 2024-12-12DOI: 10.1016/j.ceca.2024.102985
Xiao-Hua Zhang, Martin Morad
{"title":"Regulation of SR and mitochondrial Ca<sup>2+</sup> signaling by L-type Ca<sup>2+</sup> channels and Na/Ca exchanger in hiPSC-CMs.","authors":"Xiao-Hua Zhang, Martin Morad","doi":"10.1016/j.ceca.2024.102985","DOIUrl":"https://doi.org/10.1016/j.ceca.2024.102985","url":null,"abstract":"<p><strong>Rationale & methods: </strong>While signaling of cardiac SR by surface membrane proteins (I<sub>Ca</sub> & 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.</p><p><strong>Results: </strong>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 global mitochondrial Ca<sup>2+</sup> uptake, focal 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 hiPSCCMs pacing was strongly suppressed by L-type calcium channels blockers, but not by inhibiting SERCA2a by CPA.</p><p><strong>Conclusion: </strong>Spontaneous hiPSCCMs 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.</p>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"125 ","pages":"102985"},"PeriodicalIF":4.3,"publicationDate":"2024-12-12","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}
Cell calciumPub Date : 2024-12-05DOI: 10.1016/j.ceca.2024.102983
Rebecca Frank Hayward, Adam E Cohen
{"title":"All-optical mapping of Ca<sup>2+</sup> transport and homeostasis in dendrites.","authors":"Rebecca Frank Hayward, Adam E Cohen","doi":"10.1016/j.ceca.2024.102983","DOIUrl":"https://doi.org/10.1016/j.ceca.2024.102983","url":null,"abstract":"<p><p>Calcium mediates many important signals in dendrites. However, the basic transport properties of calcium in dendrites have been difficult to measure: how far and how fast does a local influx of calcium propagate? We developed an all-optical system for simultaneous targeted Ca<sup>2+</sup> import and Ca<sup>2+</sup> concentration mapping. We co-expressed a blue light-activated calcium selective channelrhodopsin, CapChR2, with a far-red calcium sensor, FR-GECO1c, in cultured rat hippocampal neurons, and used patterned optogenetic stimulation to introduce calcium into cells with user-defined patterns of space and time. We determined a mean steady-state length constant for Ca<sup>2+</sup> transport ϕ ∼ 5.8 μm, a half-life for return to baseline t<sub>1/2</sub> ∼ 1.7 s, and an effective diffusion coefficient D ∼ 20 μm<sup>2</sup>/s, though there were substantial differences in Ca<sup>2+</sup> dynamics between proximal and distal dendrites. At high Ca<sup>2+</sup> concentration, distal dendrites showed nonlinear activation of Ca<sup>2+</sup> efflux, which we pharmacologically ascribed to the NCX1 antiporter. Genetically encoded tools for all-optical mapping of Ca<sup>2+</sup> transport and handling provide a powerful capability for studying this important messenger.</p>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"125 ","pages":"102983"},"PeriodicalIF":4.3,"publicationDate":"2024-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142812032","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}
Cell calciumPub Date : 2024-12-01DOI: 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 , Refugio García-Villegas , 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}
Cell calciumPub Date : 2024-11-29DOI: 10.1016/j.ceca.2024.102980
Maria Livia Sassano, Robbe Van Gorp, Geert Bultynck, Patrizia Agostinis
{"title":"STIMulating IRE1: How store-operated Ca<sup>2+</sup> entry intersects with ER proteostasis.","authors":"Maria Livia Sassano, Robbe Van Gorp, Geert Bultynck, Patrizia Agostinis","doi":"10.1016/j.ceca.2024.102980","DOIUrl":"https://doi.org/10.1016/j.ceca.2024.102980","url":null,"abstract":"<p><p>The endoplasmic reticulum (ER) controls intracellular Ca<sup>2+</sup> dynamics. Depletion of ER Ca<sup>2+</sup> stores results in short-term activation of store-operated Ca<sup>2+</sup> entry (SOCE) via STIM1/Orai1 at ER-plasma membrane (ER-PM) contact sites (MCSs) and the long-term activation of the unfolded protein response (UPR), securing ER proteostasis. Recent work by Carreras-Sureda and colleagues describes a bidirectional control between IRE1 and STIM1 within the ER lumen that regulates ER-PM contact assembly and SOCE to sustain T-cell activation and myoblast differentiation.</p>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"125 ","pages":"102980"},"PeriodicalIF":4.3,"publicationDate":"2024-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142791115","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}
Cell calciumPub Date : 2024-11-20DOI: 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, 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}
Cell calciumPub Date : 2024-11-17DOI: 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 , Jade L. Harris , David I. Yule , James T. Slama , Jonathan S. Marchant , 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}
Cell calciumPub Date : 2024-11-16DOI: 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 , 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","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}