Cell calcium最新文献

英文中文

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 Q2 CELL BIOLOGY

Cell calcium

Pub Date : 2024-11-09 DOI: 10.1016/j.ceca.2024.102968

Mohan Manjegowda, Bimal N. Desai

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 Q2 CELL BIOLOGY

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

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 Sstr1, Sstr2, Sstr3, and Sstr5 receptor genes in a cell type-specific manner: Sstr1 and Sstr2 in thyrotrophs, Sstr3 in gonadotrophs and lactotrophs, Sstr2, Sstr3, and Sstr5 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.

体生长抑素（SST）受体家族控制着垂体激素的分泌，但这些受体在产生激素的垂体细胞的兴奋性和电压门控钙信号转导中的分布和具体作用尚未完全确定。在这里，我们发现大鼠垂体以细胞类型特异性的方式表达 Sstr1、Sstr2、Sstr3 和 Sstr5 受体基因：Sstr1和Sstr2在甲状腺营养体中表达，Sstr3在性腺营养体和泌乳营养体中表达，Sstr2、Sstr3和Sstr5在体细胞营养体中表达，而皮质营养体和黑色素营养体中没有表达。大多数性腺营养体和甲状腺营养体会自发地发射高振幅单次动作电位，SST可使其沉默而不影响细胞内钙浓度。相反，泌乳素细胞和体细胞自发地发射低幅高原爆发动作电位，同时伴有钙离子瞬态，这两种情况都被 SST 所抑制。此外，在所有表达 SST 受体的细胞类型中，SST 都能抑制 GPCR 诱导的电压门控钙信号传导和激素分泌，但在体养细胞中的抑制作用更为明显。电活动和钙信号的抑制模式与电压门控钙通道的直接和间接抑制一致，后者由细胞类型特异性超极化驱动。这些结果表明，多种类型的 SST 受体的表达及其缓慢脱敏增强了 SST 对体细胞的作用；SST 可能在性腺、甲状腺和泌乳细胞的电再同步中发挥作用；皮质和黑色素细胞中缺乏 SST 受体会使它们保持兴奋并随时准备对应激做出反应。

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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 Q2 CELL BIOLOGY

Cell calcium

Pub Date : 2024-10-29 DOI: 10.1016/j.ceca.2024.102966

Ioana Stejerean-Todoran , Christine S. Gibhardt , Ivan Bogeski

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 (Ca²⁺) 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 Ca²⁺ 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 Ca²⁺ signals to ferroptosis remains limited. Here, we summarize key connections between Ca²⁺ signaling and ferroptosis in cancer pathobiology and discuss their potential therapeutic significance.

自十多年前首次发现这种细胞死亡形式以来，铁凋亡研究领域的发展突飞猛进。铁凋亡是一种依赖于铁和 ROS 的细胞死亡形式，由多种代谢途径控制，包括但不限于氧化还原和钙（Ca2+）平衡、铁通量、线粒体功能和脂质代谢。重要的是，耐药性肿瘤特别容易受到铁氧化细胞死亡的影响，这使得铁氧化成为一种治疗多种恶性肿瘤的有前途的策略。钙信号是癌症进展和细胞死亡的重要调节因子，最近的研究表明钙信号参与了铁凋亡。发生铁突变的细胞的特点是质膜破裂并形成纳米孔，这有利于 Ca2+ 等离子流入受影响的细胞。此外，线粒体 Ca²⁺ 的水平也直接影响着细胞对铁中毒的反应。尽管该领域取得了重大进展，但我们对 Ca2+ 信号对铁变态反应的贡献的了解仍然有限。在此，我们总结了癌症病理生物学中 Ca²⁺ 信号传导与铁凋亡之间的关键联系，并讨论了它们的潜在治疗意义。

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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 Q2 CELL BIOLOGY

Cell calcium

Pub Date : 2024-10-24 DOI: 10.1016/j.ceca.2024.102965

Alexander Demby, Manuela Zaccolo

引用次数: 0

Does a transmembrane sodium gradient control membrane potential in mammalian mitochondria? 跨膜钠梯度是否能控制哺乳动物线粒体的膜电位？

IF 4.3 2区生物学 Q2 CELL BIOLOGY

Cell calcium

Pub Date : 2024-10-23 DOI: 10.1016/j.ceca.2024.102962

David G. Nicholls

In a recent publication, Hernansanz-Agusti̒n et al. propose that a sodium gradient across the inner mitochondrial membrane, generated by a Na⁺/H⁺ activity integral to Complex I can account for half of the mitochondrial membrane potential. This conflicts with conventional electrophysiological and chemiosmotic understanding.

在最近发表的一篇文章中，Hernansanz-Agusti̒n 等人提出，线粒体内膜上的钠梯度是由与复合体 I 不可分割的 Na+/H+ 活性产生的，可以占线粒体膜电位的一半。这与传统的电生理学和化学渗透理解相冲突。

引用次数: 0

Calcium and chloride out of sync: The role of signaling in Sjögren's salivary gland issues 钙和氯不同步：信号在斯约格伦唾液腺问题中的作用。

IF 4.3 2区生物学 Q2 CELL BIOLOGY

Cell calcium

Pub Date : 2024-10-21 DOI: 10.1016/j.ceca.2024.102964

Felipe Tribiños, Marcelo A. Catalan

引用次数: 0

Corrigendum to “Loss-of-function W4645R mutation in the RyR2-caffeine binding site: implications for synchrony and arrhythmogenesis” [Cell Calcium 123 (2024) 102925] RyR2-咖啡因结合位点的功能缺失W4645R突变：对同步性和心律失常发生的影响》[Cell Calcium 123 (2024) 102925]的更正。

IF 4.3 2区生物学 Q2 CELL BIOLOGY

Cell calcium

Pub Date : 2024-10-20 DOI: 10.1016/j.ceca.2024.102960

José-Carlos Fernández-Morales , Noemi Toth , Pinar Bayram , Taylor Rienzo , Martin Morad

引用次数: 0

ER stress as a sentinel mechanism for ER Ca2+ homeostasis ER应激是ER Ca2+平衡的哨兵机制。

IF 4.3 2区生物学 Q2 CELL BIOLOGY

Cell calcium

Pub Date : 2024-10-18 DOI: 10.1016/j.ceca.2024.102961

Tadashi Makio, Junsheng Chen, Thomas Simmen

Endoplasmic reticulum (ER) stress is triggered upon the interference with oxidative protein folding that aims to produce fully folded, disulfide-bonded and glycosylated proteins, which are then competent to exit the ER. Many of the enzymes catalyzing this process require the binding of Ca²⁺ ions, including the chaperones BiP/GRP78, calnexin and calreticulin. The induction of ER stress with a variety of drugs interferes with chaperone Ca²⁺ binding, increases cytosolic Ca²⁺through the opening of ER Ca²⁺ channels, and activates store-operated Ca²⁺ entry (SOCE). Posttranslational modifications (PTMs) of the ER Ca²⁺ handling proteins through ER stress-dependent phosphorylation or oxidation control these mechanisms, as demonstrated in the case of the sarco/endoplasmic reticulum ATPase (SERCA), inositol 1,4,5 trisphosphate receptors (IP₃Rs) or stromal interaction molecule 1 (STIM1). Their aim is to restore ER Ca²⁺ homeostasis but also to increase Ca²⁺ transfer from the ER to mitochondria during ER stress. This latter function boosts ER bioenergetics, but also triggers apoptosis if ER Ca²⁺ signaling persists. ER Ca²⁺ toolkit oxidative modifications upon ER stress can occur within the ER lumen or in the adjacent cytosol. Enzymes involved in this redox control include ER oxidoreductin 1 (ERO1) or the thioredoxin-family protein disulfide isomerases (PDI) and ERp57. A tight, but adaptive connection between ER Ca²⁺ content, ER stress and mitochondrial readouts allows for the proper functioning of many tissues, including skeletal muscle, the liver, and the pancreas, where ER stress either maintains or compromises their function, depending on its extent and context. Upon mutation of key regulators of ER Ca²⁺ signaling, diseases such as muscular defects (e.g., from mutated selenoprotein N, SEPN1/SELENON), or diabetes (e.g., from mutated PERK) are the result.

内质网（ER）应激是在氧化蛋白质折叠受到干扰时引发的，目的是产生完全折叠、二硫键结合和糖基化的蛋白质，然后使其能够离开ER。催化这一过程的许多酶都需要与 Ca2+ 离子结合，其中包括伴侣蛋白 BiP/GRP78、calnexin 和 calreticulin。用多种药物诱导ER应激会干扰伴侣的Ca2+结合，通过打开ER Ca2+通道增加细胞膜Ca2+，并激活贮存操作的Ca2+进入（SOCE）。ER钙离子处理蛋白的翻译后修饰（PTM）是通过ER应激依赖性磷酸化或氧化来控制这些机制的，如肌浆/内质网ATP酶（SERCA）、1,4,5-三磷酸肌醇受体（IP3Rs）或基质相互作用分子1（STIM1）的情况所示。它们的目的是恢复 ER Ca2+ 的平衡，同时在 ER 应激时增加 Ca2+ 从 ER 向线粒体的转移。后一种功能可增强 ER 的生物能，但如果 ER Ca2+ 信号持续存在，也会引发细胞凋亡。ER应激时ER Ca2+工具箱的氧化修饰可发生在ER腔内或邻近的细胞质中。参与这种氧化还原控制的酶包括ER氧化还原蛋白1（ERO1）或硫氧还原蛋白家族的蛋白二硫异构酶（PDI）和ERp57。ER Ca2+ 含量、ER 应激和线粒体读数之间存在着紧密的适应性联系，这使得包括骨骼肌、肝脏和胰腺在内的许多组织都能正常运作。一旦ER Ca2+信号的关键调节因子发生突变，就会导致肌肉缺陷（如硒蛋白N SEPN1/SELENON突变）或糖尿病（如PERK突变）等疾病。

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引用次数: 0

The IP3 receptor-KRAP complex at the desmosomes: A new player in the apoptotic process 脱粘体上的 IP3 受体-KRAP 复合物：凋亡过程中的新角色

IF 4.3 2区生物学 Q2 CELL BIOLOGY

Cell calcium

Pub Date : 2024-10-18 DOI: 10.1016/j.ceca.2024.102963

Jan B. Parys

The IP₃ receptor (IP₃R) is a ubiquitously expressed Ca²⁺-release channel located in the endoplasmic reticulum (ER). Ca²⁺ signals originating from the IP₃R initiate or regulate a plethora of cellular events, including cell life and death processes, e.g. exaggerated Ca²⁺ release from the ER to the mitochondria is a trigger for apoptosis. Recently, Cho et al. (Current Biology, 2024, DOI: 10.1016/j.cub.2024.08.057) demonstrated that in epithelial monolayers a sustained [Ca²⁺] elevation caused by the IP₃Rs is responsible for the extrusion of adjacent apoptotic cells out of the epithelial monolayer. Interestingly, the IP₃Rs involved are associated with the desmosomes via K-Ras-induced actin-interacting protein (KRAP). This study not only highlight a novel role of the IP₃R in apoptosis, but also shed a new light on how KRAP -and by extension KRAP-related proteins- contribute to the regulation of IP₃R activity and, more broadly, underscores the crucial role of associated proteins in determining the function of IP₃Rs.

IP3 受体（IP3R）是一种普遍表达的 Ca2+ 释放通道，位于内质网（ER）中。源自 IP3R 的 Ca2+ 信号可启动或调控大量细胞事件，包括细胞的生死过程，例如，从 ER 向线粒体释放过量 Ca2+ 可触发细胞凋亡。最近，Cho 等人（《当代生物学》，2024 年，DOI: 10.1016/j.cub.2024.08.057）证实，在上皮单层中，由 IP3Rs 引起的持续[Ca2+]升高是相邻凋亡细胞挤出上皮单层的原因。有趣的是，参与其中的 IP3R 通过 K-Ras 诱导的肌动蛋白相互作用蛋白（KRAP）与脱钙小体相关联。这项研究不仅凸显了 IP3R 在细胞凋亡中的新作用，而且还揭示了 KRAP 以及 KRAP 相关蛋白如何促进 IP3R 活性的调节，更广泛地说，它强调了相关蛋白在决定 IP3R 功能方面的关键作用。

引用次数: 0

MICU1 and MICU2, two peas in a pod or entirely different fruits? MICU1 和 MICU2 是一个豆荚里的两颗豆子，还是完全不同的果实？

IF 4.3 2区生物学 Q2 CELL BIOLOGY

Cell calcium

Pub Date : 2024-10-08 DOI: 10.1016/j.ceca.2024.102959

Jiuzhou Huo, Jeffery D. Molkentin

Fluctuations in mitochondrial matrix Ca²⁺ plays a critical role in matching energy production to cellular demand through direct effects on oxidative phosphorylation and ATP production. Disruption in mitochondrial Ca²⁺ homeostasis, particularly under pathological conditions such as ischemia or heart failure, can lead to mitochondrial dysfunction, energy deficit, and eventually death of cardiomyocytes. The primary channel regulating acute mitochondrial Ca²⁺ influx is the mitochondrial Ca²⁺ uniporter (mtCU), which is regulated by the mitochondrial Ca²⁺ uptake (MICU) proteins that were examined here.

线粒体基质 Ca2+ 的波动通过直接影响氧化磷酸化和 ATP 的产生，在使能量产生与细胞需求相匹配方面发挥着至关重要的作用。线粒体 Ca2+ 平衡的破坏，尤其是在缺血或心力衰竭等病理情况下，可导致线粒体功能障碍、能量不足，并最终导致心肌细胞死亡。调节急性线粒体 Ca2+ 流入的主要通道是线粒体 Ca2+ 单通道（mtCU），它受线粒体 Ca2+ 摄取（MICU）蛋白的调节。

引用次数: 0

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Cell calcium

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