Cell calcium最新文献

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Rapid quantification of intracellular calcium stores reveals effects of membrane micropeptides on SERCA function

IF 4.3 2区生物学 Q2 CELL BIOLOGY

Cell calcium

Pub Date : 2025-02-07 DOI: 10.1016/j.ceca.2025.103000

Jacob D. Cunningham, Taylor A. Phillips, Jaroslava Seflova, Ellen E. Cho, Seth L. Robia

To determine how regulation of the sarco(endo)plasmic reticulum calcium ATPase (SERCA) affects the Ca²⁺ content of the endoplasmic reticulum (ER), we developed a ratiometric ER-localized Ca²⁺ indicator to rapidly quantify Ca²⁺ stores and assess SERCA function in live cells. This assay enables screening of membrane micropeptides and small molecules that modulate SERCA and Na⁺/K⁺-ATPase activity and may facilitate development of therapies that target cellular Ca²⁺ handling. Of the micropeptides tested, phospholamban (PLB) had the greatest degree of inhibition of SERCA, as measured by a decrease in ER Ca²⁺ content compared to control. Sarcolipin (SLN), endoregulin (ELN), and another-regulin (ALN) also decreased ER Ca²⁺ content, though less potently than PLB. We also investigated micropeptides that have been shown to have a positive effect on ER Ca²⁺ uptake. Dwarf open reading frame (DWORF), a positive modulator of SERCA activity, and phospholemman (PLM), an inhibitor of the Na⁺/K⁺-ATPase, both increased ER Ca²⁺ content compared to control. A superinhibitory variant of PLM, R70C, further increased ER Ca²⁺ load compared to wild type PLM. Overall, our findings indicate that the inhibitory potency of micropeptides is governed by their relative binding affinities to SERCA. This allows for finely tuned modulation of Ca²⁺ handling in different tissues based on differential expressions of micropeptide species. Understanding the contribution of each micropeptide to SERCA regulation may reveal novel strategies for therapeutic intervention in conditions where calcium dysregulation plays a role, such as heart disease, vascular disease, or neurodegenerative disorders.

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Shocking insights for neurovascular coupling: Electrical signals ignite calcium dynamics in brain capillaries

IF 4.3 2区生物学 Q2 CELL BIOLOGY

Cell calcium

Pub Date : 2025-02-01 DOI: 10.1016/j.ceca.2025.103001

Boris Lavanderos , Maria Paz Saldias , Scott Earley

Brain capillaries contribute to neurovascular coupling (NVC) by sensing neural activity and coordinating upstream arteriole dilation. However, the mechanisms underlying conducted vasodilation remain incompletely understood. Recent findings (PNAS, 2024) identify a novel process, “electrocalcium coupling,” in which hyperpolarizing signals from K⁺ channels drive long-range Ca²⁺ signaling in capillaries, revealing new insights into the integration of vasodilatory signals in the brain.

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You better keep an eye on your contacts

IF 4.3 2区生物学 Q2 CELL BIOLOGY

Cell calcium

Pub Date : 2025-01-22 DOI: 10.1016/j.ceca.2025.102999

Tamas Balla, Gergo Gulyas

Membrane contact sites (MCS) are specialized compartments found in all eukaryotic cells that are formed between membranes of different organelles that are in close proximity. MCS have important functions as they are sites of efficient transfer of molecules between neighboring organelles. Two recent articles have used the splitFAST system to mark and follow the dynamics of membrane contact sites and used the method to highlight the importance of MCS between the endoplasmic reticulum (ER) and lipid droplets in metabolic adaptation and MCS between the ER and mitochondria in Ca²⁺ signal propagation.

引用次数: 0

Commentary to An Orai1 gain-of-function tubular aggregate myopathy mouse model phenocopies key features of the human disease (Zhao et al., EMBO Journal 2024) and A gain-of-function mutation in the Ca2+ channel ORAI1 causes Stormorken syndrome with tubular aggregates in mice (Pérez-Guàrdia et al., Cells 2024)

IF 4.3 2区生物学 Q2 CELL BIOLOGY

Cell calcium

Pub Date : 2025-01-21 DOI: 10.1016/j.ceca.2025.102998

Johann Böhm

引用次数: 0

Ionic signalling (beyond calcium) in the nervous system: Physiology and pathophysiology 神经系统中的离子信号（除钙外）：生理学和病理生理学。

IF 4.3 2区生物学 Q2 CELL BIOLOGY

Cell calcium

Pub Date : 2025-01-01 DOI: 10.1016/j.ceca.2024.102984

Verena Untiet , Chritsine R. Rose , Maiken Nedergaard , Alexei Verkhratsky

引用次数: 0

STIMulating IRE1: How store-operated Ca2+ entry intersects with ER proteostasis 刺激IRE1：储存操作的Ca2+进入如何与内质网蛋白酶平衡相交。

IF 4.3 2区生物学 Q2 CELL BIOLOGY

Cell calcium

Pub Date : 2025-01-01 DOI: 10.1016/j.ceca.2024.102980

Maria Livia Sassano , Robbe Van Gorp , Geert Bultynck , Patrizia Agostinis

The endoplasmic reticulum (ER) controls intracellular Ca²⁺ dynamics. Depletion of ER Ca²⁺ stores results in short-term activation of store-operated Ca²⁺ 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.

内质网（ER）控制着细胞内 Ca2+ 的动态变化。ER Ca2+ 储存的耗竭会导致通过ER-质膜（ER-PM）接触点（MCSs）上的 STIM1/Orai1 短期激活储存操作的 Ca2+ 进入（SOCE），并长期激活未折叠蛋白反应（UPR），从而确保ER的蛋白稳态。Carreras-Sureda 及其同事最近的研究描述了ER腔内IRE1和STIM1之间的双向控制，这种控制调节ER-PM接触组装和SOCE，以维持T细胞活化和成肌细胞分化。

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A role for lysosomal calcium channels in mitigating mitochondrial damage and oxidative stress 溶酶体钙通道在减轻线粒体损伤和氧化应激中的作用。

IF 4.3 2区生物学 Q2 CELL BIOLOGY

Cell calcium

Pub Date : 2025-01-01 DOI: 10.1016/j.ceca.2024.102986

Leandro C. Clementino , Andrew P. Thomas , Emily M. Rocha , Sabine Hilfiker

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 Ca²⁺ channel may be a viable option to alleviate oxidative damage by boosting lysosome biogenesis and mitophagy.

游离脂肪酸升高和氧化应激可能是与各种心血管并发症相关的内皮功能障碍的致病因素。在最近的研究中，Feng和他的同事报告说，激活溶酶体Ca2+通道可能是一种可行的选择，可以通过促进溶酶体的生物发生和线粒体自噬来减轻氧化损伤。

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TPC2 controls MITF expression and metastasis in melanoma TPC2控制黑色素瘤中MITF的表达和转移。

IF 4.3 2区生物学 Q2 CELL BIOLOGY

Cell calcium

Pub Date : 2025-01-01 DOI: 10.1016/j.ceca.2024.102989

M. Raza Zaidi , Jonathan Soboloff

Recent findings by Abrahamian et al. (2024) provides new insights into the relationship between Two Pore Channel 2 (TPC2) activity and the development and progression of melanoma. Melanocyte inducing transcription factor (MITF) is a critical regulator of both melanocyte and melanoma behavior. Abrahamian et al. (2024) show that MITF-high melanoma requires BOTH Rab7a and TPC2 for proliferation, invasion and metastasis. They further identify Wnt signaling as the mediator of this phenomenon; Rab7a induces TPC2 activity in lysosomes and melanosomes, which regulates GSK-3β stability, thereby determining whether β-catenin escapes degradation and translocates to the nucleus to transcribe the MITF gene. These observations provide new insights into the relationship between ion channel function, lysosomal/melanosomal activity and control for oncogenesis and disease progression in melanoma.

Abrahamian等人（2024）的最新发现为双孔通道2 （Two Pore Channel 2, TPC2）活性与黑色素瘤的发生和发展之间的关系提供了新的见解。黑素细胞诱导转录因子（MITF）是黑素细胞和黑色素瘤行为的关键调节因子。Abrahamian等（2024）发现mitf高的黑色素瘤的增殖、侵袭和转移都需要Rab7a和TPC2。他们进一步确定Wnt信号是这一现象的中介；Rab7a诱导溶酶体和黑素小体中的TPC2活性，从而调节GSK-3β的稳定性，从而决定β-catenin是否逃脱降解并易位到细胞核中转录MITF基因。这些观察结果为离子通道功能、溶酶体/黑素体活性与黑色素瘤发生和疾病进展的控制之间的关系提供了新的见解。

引用次数: 0

Ca²⁺ signaling in myenteric interstitial cells of Cajal (ICC-MY) and their role as conditional pacemakers in the colon ca2 +在Cajal肌间质细胞（ICC-MY）中的信号传导及其在结肠中作为条件起搏器的作用。

IF 4.3 2区生物学 Q2 CELL BIOLOGY

Cell calcium

Pub Date : 2025-01-01 DOI: 10.1016/j.ceca.2024.102990

Salah A. Baker , Manushri Karwa , Ji Yeon Lee , Sarah Riar , Bernard T. Drumm , Kenton M. Sanders

Interstitial cells of Cajal in the plane of the myenteric plexus (ICC-MY) serve as electrical pacemakers in the stomach and small intestine. A similar population of cells is found in the colon, but these cells do not appear to generate regular slow wave potentials, as characteristic in more proximal gut regions. Ca²⁺ handling mechanisms in ICC-MY of the mouse proximal colon were studied using confocal imaging of muscles from animals expressing GCaMP6f exclusively in ICC. ICC-MY displayed stochastic, localized Ca²⁺ transients that seldom propagated between cells. Colonic ICC express ANO1 channels, so Ca²⁺ transients likely couple to activation of spontaneous transient inward currents (STICs) in these cells. The Ca²⁺ transients were due to Ca²⁺ release and blocked by cyclopiazonic acid (CPA), thapsigargin and caffeine, but unaffected by tetracaine. Antagonists of L- and T-type Ca²⁺ channels and reduction in extracellular Ca²⁺ had minimal effects on Ca²⁺ transients. We reasoned that STICs may not activate regenerative Ca²⁺ waves in ICC-MY because voltage-dependent Ca²⁺ conductances are largely inactivated at the relatively depolarized potentials of colonic muscles. We tested the effects of hyperpolarization with pinacidil, a K_ATP agonist. Ca²⁺ waves were initiated in some ICC-MY networks when muscles were hyperpolarized, and these events were blocked by a T-type Ca²⁺ channel antagonist, NNC 55–0396. Ca²⁺ waves activated by excitatory nerve stimulation were significantly enhanced by hyperpolarization. Our data suggest that colonic ICC-MY are conditional pacemaker cells that depend upon preparative hyperpolarization, produced physiologically by inputs from enteric inhibitory neurons and necessary for regenerative pacemaker activity.

肌丛平面Cajal间质细胞（ICC-MY）在胃和小肠中起电起搏器的作用。在结肠中也发现了类似的细胞群，但这些细胞似乎不能产生规律的慢波电位，这是更近端肠道区域的特征。通过在ICC中表达GCaMP6f的动物的肌肉共聚焦成像，研究了小鼠近端结肠ICC- my中的Ca2+处理机制。ICC-MY表现出随机的、局部的Ca2+瞬态，很少在细胞间繁殖。结肠ICC表达ANO1通道，因此Ca2+瞬态可能与这些细胞中的自发瞬态内向电流（tics）激活偶联。Ca2+瞬态是由于Ca2+释放，并被环吡唑酸（CPA）， thapsigargin和咖啡因阻断，但不受丁卡因影响。L型和t型Ca2+通道的拮抗剂和细胞外Ca2+的减少对Ca2+瞬态的影响最小。我们推断，tic可能不会激活ICC-MY中的再生Ca2+波，因为电压依赖性Ca2+电导在结肠肌肉的相对去极化电位下大部分失活。我们用pinacidil（一种KATP激动剂）测试了超极化的效果。当肌肉处于超极化状态时，Ca2+波在一些cc - my网络中启动，这些事件被t型Ca2+通道拮抗剂NNC 55-0396阻断。超极化显著增强兴奋性神经刺激激活的Ca2+波。我们的数据表明，结肠ICC-MY是条件性起搏器细胞，依赖于准备性超极化，由肠抑制神经元输入产生，是再生起搏器活动所必需的。

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引用次数: 0

ROS and calcium signaling are critical determinant of skin pigmentation 活性氧和钙信号是皮肤色素沉着的关键决定因素。

IF 4.3 2区生物学 Q2 CELL BIOLOGY

Cell calcium

Pub Date : 2025-01-01 DOI: 10.1016/j.ceca.2024.102987

Kriti Ahuja, Sharon Raju, Sakshi Dahiya, Rajender K Motiani

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 (Ca²⁺) signaling modules regulate physiological pigmentation. Further, pigmentary disorders are associated with dysregulated ROS homeostasis and changes in Ca²⁺ dynamics. Here, we systemically review the literature that demonstrates key role of ROS and Ca²⁺ signaling in pigmentation and pigmentary disorders. Further, we discuss recent studies, which have revealed that organelle-specific Ca²⁺ 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 Ca²⁺ 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 Ca²⁺ 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 Ca²⁺ signaling to human pigmentary disorders.

色素沉着是一种保护现象，可以保护皮肤细胞免受紫外线引起的DNA损伤。色素沉着途径的扰动易患皮肤癌并导致色素紊乱。这些疾病会造成心理创伤，严重影响患者的生活质量。新出现的文献表明活性氧（ROS）和钙（Ca2+）信号模块调节生理色素沉着。此外，色素紊乱与活性氧稳态失调和Ca2+动力学变化有关。在这里，我们系统地回顾了证明ROS和Ca2+信号在色素沉着和色素紊乱中的关键作用的文献。此外，我们讨论了最近的研究，这些研究揭示了细胞器特异性Ca2+运输机制是色素沉着的关键决定因素。重要的是，我们考虑通过治疗靶向ROS生成和细胞Ca2+处理工具包临床管理色素紊乱的可能性。最后，我们强调了该领域需要关键和及时关注的关键突出问题。虽然ROS和Ca2+信号在调节皮肤色素沉着中的重要作用已经出现，但其潜在的分子机制仍然知之甚少。未来，详细研究连接ROS稳态紊乱和Ca2+信号与人类色素紊乱的信号级联将是至关重要的。

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