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Macronutrients
Published in Chuong Pham-Huy, Bruno Pham Huy, Food and Lifestyle in Health and Disease, 2022
Chuong Pham-Huy, Bruno Pham Huy
Sphingolipids constitute a class of lipids defined by their 18 carbon-amino-alcohol backbones which are synthesized in the endoplasmic reticulum from non-sphingolipid precursors (66, 117). In sphingolipids, glycerol is replaced by a group of aliphatic amino alcohol named sphingosine that contains two alcohols with the middle position occupied by an amine. Sphingolipids are complex lipids which yield fatty acids, sphingosine, phosphoric acid, and an alcohol component upon hydrolysis. A sphingosine has three parts, a three carbon chain with two alcohols and amine attached and a long hydrocarbon chain containing 12–22 carbon atoms (69, 115, 117). The main and abundant component of sphingolipids in animals is sphingomyelin that constitutes the membranous myelin sheath surrounding nerve cell axons (114, 117). Sphingomyelin usually consists of a sphingosine linked to a long chain fatty acyl chain called ceramide and attached to a phosphocholine group at the primary alcohol group of a sphingosine (66, 117). Precisely, ceramide is amide of fatty acids with sphingosine. So, sphingomyelin can also be classified as sphingophospholipid (115). Like glycerophospholipids and cholesterol, sphingolipids are ubiquitous in the body and found in every cell membrane, particularly nerve cells and brain tissues (114–117).
Endotoxic Shock and the Sphingomyelin Pathway
Published in Helmut Brade, Steven M. Opal, Stefanie N. Vogel, David C. Morrison, Endotoxin in Health and Disease, 2020
Cecil K. Joseph, Richard N. Kolesnick
The sphingomyelin pathway appears to be evolution-arily conserved and functions in nearly all mammalian cells. This pathway is often initiated when a ligand binds to a specific cell surface receptor, leading to the activation of one or more sphingomyelinases (SMases), sphingomyelin-specific forms of phospholipase C, that hydrolyze the phosphodiester bond of sphingomyelin yielding ceramide and phosphorylcholine. Alternatively, the pathway can be activated in a receptor-independent fashion by environmental stresses such as ionizing radiation, heat, oxidative stress, and ultraviolet light. Several isoforms of SMase, distinguished by their pH optima, exist in human and murine cells. Human and murine acid (A)-SMases (pH optimum 4.5–5.0) were originally localized to lysosomal and endosomal compartments. However, A-SMase activity has been measured in the caveolae of cells treated with IL-1 and nerve growth factor (NGF) (11) and recently as a secretory product of endothelial cells (12,13). Patients suffering from the inherited disorder Nieman-Pick disease (NPD) are deficient in A-SMase activity due to a variety of known point mutations in the A-SMase gene (14).
Acute Alveolar Injury: Experimental Models
Published in Joan Gil, Models of Lung Disease, 2020
Purified surfactants from lungs during early (2-4 day) and peak (6-8 day) injury failed to lower surface tension below 20 dynes/cm when spread as films and compressed on a modified Wilhelmy balance even when excess material was applied to the surface, whereas those from lungs after recovery were not different from those from control animals (Fig. 36). During early recovery (day 10-12), surface tensions were lowered to levels intermediate between those at peak injury and those after recovery. In addition, the rate of adsorption of surfactant into the surface film from the hypophase was decreased during early and peak injury and returned to normal during recovery. Analysis of phospholipids and neutral lipids of the purified surfactant (Table 3) revealed that the percentages of all the major phospholipids except PG in all phases of injury and recovery were not different from those of control animals. PG decreased markedly during injury and remained at minimal levels throughout recovery while both PI and lysophosphatidylcholine behaved reciprocally with PG, increasing and remaining increased during injury and recovery. An increase in sphingomyelin (SPH) led to a reduced PC/SPH (L/S) ratio.
What can we learn from the platelet lipidome?
Published in Platelets, 2023
Gaëtan Chicanne, Jean Darcourt, Justine Bertrand-Michel, Cédric Garcia, Agnès Ribes, Bernard Payrastre
However, whether specific platelet lipidomic profiles may become diseases signature remains to be established. Moreover, how altered platelet lipidome can be involved in platelet-dependent pathologies is still poorly understood. Yet, some inherited pathologies are directly linked to platelet lipid modifications. This includes the loss of PS exposure due to TMEM16F scramblase mutations impairing the procoagulant function of platelets in the bleeding Scott syndrome [32], the rare inherited cPLA2 deficiency leading to platelet dysfunction [21], the decreased expression of PLCβ2 linked to hypo-responsive platelets [33], or the loss of function of the PI(4,5)P2 5-phosphatase affecting platelet responses in the LOWE syndrome [34]. Some mouse models have also pointed to new important lipid-related pathways that should stimulate to prioritize a lipidomic analysis in patients. For instance, as mentioned above, mice lacking sphingomyelin phosphodiesterase 1 have platelet dysfunction suggesting that human platelets deficient in this enzyme, such as platelets from Niemann-Pick patients, may be affected. A mouse model of sitosterolemia caused by a mutation in the ABCG5 or ABCG8 transporter genes has linked the accumulation of free plant sterols in platelet membranes to dysregulation of platelet functions leading to macrothrombocytopenia and bleeding [35]. Lipidomic studies on platelets from sitosterolemia patients should bring interesting information as well as potential diagnostic and disease monitoring markers.
Outcome measures and biomarkers in chronic inflammatory demyelinating polyradiculoneuropathy: from research to clinical practice
Published in Expert Review of Neurotherapeutics, 2021
Jeffrey A. Allen, Filip Eftimov, Luis Querol
There is no known biomarker that reliably reflects myelin damage. Plasma levels of the Schwann cell-specific transmembrane protease serine 5 protein (TMPRSS5) were shown to be significantly elevated in Charcot-Marie-Tooth disease [56]; however, its role as a biomarker in acquired demyelinating neuropathies is unknown. There is some evidence that CSF sphingomyelin, a myelin-enriched lipid, may be a useful diagnostic and disease activity biomarker. Diagnostically, sensitivity (80.8%) and specificity (98.8%) in patients with acute and chronic demyelinating polyradiculoneuropathies is favorable. CSF sphingomyelin also has been shown to be higher in patients with active CIDP compared to those with stable disease and compared to axonal controls, suggesting its potential role as a disease activity biomarker [57]. Further study of CSF sphingomyelin in large cohorts of patients at various stages of disease is needed before it can be adopted into routine clinical care.
Biological membranes in EV biogenesis, stability, uptake, and cargo transfer: an ISEV position paper arising from the ISEV membranes and EVs workshop
Published in Journal of Extracellular Vesicles, 2019
Ashley E. Russell, Alexandra Sneider, Kenneth W. Witwer, Paolo Bergese, Suvendra N. Bhattacharyya, Alexander Cocks, Emanuele Cocucci, Uta Erdbrügger, Juan M. Falcon-Perez, David W. Freeman, Thomas M. Gallagher, Shuaishuai Hu, Yiyao Huang, Steven M. Jay, Shin-ichi Kano, Gregory Lavieu, Aleksandra Leszczynska, Alicia M. Llorente, Quan Lu, Vasiliki Mahairaki, Dillon C. Muth, Nicole Noren Hooten, Matias Ostrowski, Ilaria Prada, Susmita Sahoo, Tine Hiorth Schøyen, Lifu Sheng, Deanna Tesch, Guillaume Van Niel, Roosmarijn E. Vandenbroucke, Frederik J. Verweij, Ana V. Villar, Marca Wauben, Ann M. Wehman, Hang Yin, David Raul Francisco Carter, Pieter Vader
Sphingomyelin is a sphingolipid normally found in the outer leaflet of membranes (extracellular or luminal side). Enzymes such as neutral sphingomyelinase (nSMase) and acid sphingomyelinase (aSMase) convert sphingomyelin into phosphocholine and ceramide, which alters membrane fluidity and promotes microdomain formation. Interestingly, 62% of survey respondents believe that lipid rafts/microdomains contribute to the formation of vesicles [69,70] (Figure 6). nSMase inhibitors, such as GW4869, have been shown to significantly reduce small EV release from some [71], but not all systems [72], and even results in a compensatory increase in large EVs in some systems [73]. Conversely, overexpressing nSMase2 increases ILV formation, which is thought to occur via an ESCRT-independent biogenesis pathway [71]. More than half (59%) of ISEV workshop participants doubted nSMase2 involvement in the biogenesis of all EV subtypes (Figure 6), but there is also evidence that aSMases are involved in EV release [74]. Thus, the roles of various sphingomyelinases, ceramide, and lipid rafts in EV biogenesis require further investigation.