Metabolites of sphingomyelin, as well as calcium ion fluxes, have a profound role in cellular signaling in almost all cell types. In addition, metabolites of sphingomyelin often modulate calcium signaling, either directly or indirectly. This is an interesting aspect on how lipids may wield their physiological role, as calcium is probably one of the most versatile signaling molecules in the cell, and as modulation of calcium signaling has profound effects on cellular physiology. The aim of this review is to discuss the mechanisms by which metabolites of sphingomyelin, especially the sphingolipids sphingosine and sphingosine 1-phosphate (S1P), modulate calcium fluxes, and how this may affect cellular function. In addition, the pathological aspects of sphingolipid-evoked modulation of calcium fluxes will be discussed.
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http://dx.doi.org/10.1016/j.bbamcr.2018.04.012 | DOI Listing |
Adv Sci (Weinh)
January 2025
Medical 3D Printing Center, Orthopedic Institute, Department of Orthopedic Surgery, The First Affiliated Hospital, School of Basic Medical Sciences, MOE Key Laboratory of Geriatric Diseases and Immunology, Suzhou Medical College, Soochow University, Suzhou, Jiangsu, 215000, China.
Stem cell implantation holds promise for enhancing bone repair, but risks of pathogen transmission and malignant cell transformation should not be ignored. Compared to stem cell implantation, recruitment of endogenous stem cells to injured sites is more critical for in situ bone regeneration. In this study, based on the acidic microenvironment of bone injury, an HG-AA-SDF-1α composite hydrogel with a dual-control intelligent switch function is developed by incorporating stromal cell-derived factor (SDF-1α), arginine carbon dots (Arg-CDs), and calcium ions (Ca) into the oxidized hyaluronic acid/gelatin methacryloyl (HG) hydrogel.
View Article and Find Full Text PDFPotassium channels regulate membrane potential, calcium flux, cellular activation and effector functions of adaptive and innate immune cells. The voltage-activated Kv1.3 channel is an important regulator of T cell-mediated autoimmunity and microglia-mediated neuroinflammation.
View Article and Find Full Text PDFFront Neurosci
January 2025
Department of Neurophysiology, Instituto Nacional de Neurología y Neurocirugía "Manuel Velasco Suárez", Mexico City, Mexico.
The interplay between long-term potentiation (LTP) and epilepsy represents a crucial facet in understanding synaptic plasticity and memory within neuroscience. LTP, a phenomenon characterized by a sustained increase in synaptic strength, is pivotal in learning and memory processes, particularly in the hippocampus. This review delves into the intricate relationship between LTP and epilepsy, exploring how alterations in synaptic plasticity mechanisms akin to those seen in LTP contribute to the hyperexcitable state of epilepsy.
View Article and Find Full Text PDFNeurophotonics
January 2025
Northeastern University, Department of Bioengineering, Boston, Massachusetts, United States.
Significance: Functional brain imaging experiments in awake animals require meticulous monitoring of animal behavior to screen for spontaneous behavioral events. Although these events occur naturally, they can alter cell signaling and hemodynamic activity in the brain and confound functional brain imaging measurements.
Aim: We developed a centralized, user-friendly, and stand-alone platform that includes an animal fixation frame, compact peripheral sensors, and a portable data acquisition system.
Adv Sci (Weinh)
January 2025
Clinical Research Center, Postdoctoral Station of Clinical Medicine, The Third Xiangya Hospital, Central South University, Changsha, 410013, P. R. China.
Vascular calcification is a highly regulated process in cardiovascular disease (CVD) and is strongly correlated with morbidity and mortality, especially in the adverse stage of vascular remodeling after coronary artery bypass graft surgery (CABG). However, the pathogenesis of vascular graft calcification, particularly the role of endothelial-smooth muscle cell interaction, is still unclear. To test how ECs interact with SMCs in artery grafts, single-cell analysis of wild-type mice is first performed using an arterial isograft mouse model and found robust cytokine-mediated signaling pathway activation and SMC proliferation, together with upregulated endothelial tripartite motif 35 (TRIM35) expression.
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