Effects of divalent cations on lipid flip-flop in the human erythrocyte membrane

Henseleit, U.; Plasa, G.; Haest, C.W.M.

doi:10.1016/0005-2736(90)90445-t

Cited by 53 publications

(32 citation statements)

References 40 publications

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“…Increase in cytosolic Ca 2 + by addition of Ca 2 + and ionophore strongly stimulates lipid scrambling, which is accompanied by vesicle shedding (22). Similar observations were made with erythrocytes, although the lipid scrambling triggered by cytosolic Ca2+ is less efficient (19,22,24,59). Importantly, not only PS but PE also flops to the outer monolayer while PC flips inside.…”

Section: Protein Involvement In Transmembrane Lipid Passagesupporting

confidence: 67%

“…Alternatively, partial disturbances of the bilayer structure could occur during fusion of the granules that accompanies in some instances platelet stimulation or during fusion of the plasma membrane that takes place upon shedding of membrane micro vesicles (22). The Ca2+ pathway for lipid scrambling persists as long as cytosolic Ca 2 + remains elevated, and disappears promptly when Ca 2 + levels fail (P. Williamson (8,59). So, in conclusion, the mech anism of this fast lipid scrambling is far from being understood.…”

Section: Protein Involvement In Transmembrane Lipid Passagementioning

confidence: 99%

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Protein Involvement in Transmembrane Lipid Asymmetry

Devaux

1992

Annu. Rev. Biophys. Biomol. Struct.

186

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Transmembrane asymmetry has been extensively studied in eukaryotic cells. It is as yet only clearly demonstrated in the plasma membrane of a few cells. Subcellular organelles have evidence of lipid asymmetry, but very little consistent quantitative data exist. Proteins involved in transmembrane passage of lipids comprise enzymes of lipid metabolism and also the so-called phospholipid flippases that are either passive or active putative lipid transporters. The aminophospholipid translocase that pumps amino-phospholipids from the outer to the inner monolayer of the plasma membrane of eukaryotes is a Mg(2+)-ATP dependent protein with a high lipid selectivity. Lipid asymmetry provides an asymmetrical environment for membrane enzymes. Thus, PS (and PE) reorientation could be a way of controlling or triggering specific enzymes. Also, the asymmetrical distribution of phospholipids most likely determines the fusion-competent membranes and/or which sides of membranes should fuse. Finally, the lipid pump as well as all enzymes responsible for the net transmembrane flux of phospholipids may provide the driving force for membrane bending, notably during the formation of endocytic vesicles. Clearly, real progress in this area will be made only if the proteins of the flippase family are purified and antibodies obtained that will permit the recognition and localization of these proteins in various cells. Also, specific inhibitors as well as mutants would allow one to infer more directly what are the real functions of these proteins. At a late stage, the protein purification will eventually permit speculation on the mechanism of action of a pump that must transport simultaneously hydrophilic and hydrophobic groups through a membrane.

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Section: Protein Involvement In Transmembrane Lipid Passagesupporting

confidence: 67%

Section: Protein Involvement In Transmembrane Lipid Passagementioning

confidence: 99%

Protein Involvement in Transmembrane Lipid Asymmetry

Devaux

1992

Annu. Rev. Biophys. Biomol. Struct.

186

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“…Notably, membrane remodeling and PS externalization is dependent on an increase in cytosolic calcium. 55 Activation of human platelets by a Ca 2ϩ ionophore results in the surface exposure of PS. Conversely, the inhibition of Ca 2ϩ influx abolishes agonist-induced PS externalization and the procoagulant response in activated platelets.…”

Section: Calcium Channels Ions and Microparticle Formationmentioning

confidence: 99%

Cellular Mechanisms Underlying the Formation of Circulating Microparticles

Morel

Jesel

Freyssinet

et al. 2011

ATVB

473

405

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Abstract-Microparticles (MPs) derived from platelets, monocytes, endothelial cells, red blood cells, and granulocytes may be detected in low concentrations in normal plasma and at increased levels in atherothrombotic cardiovascular diseases. The elucidation of the cellular mechanisms underlying the generation of circulating MPs is crucial for improving our understanding of their pathophysiological role in health and disease. The flopping of phosphatidylserine (PS) to the outer leaflet of the plasma membrane is the key event that will ultimately lead to the shedding of procoagulant MPs from activated or apoptotic cells. Research over the last few years has revealed important roles for calcium-, mitochondrial-, and caspase-dependent mechanisms leading to PS exposure. The study of Scott cells has unraveled different molecular mechanisms that may contribute to fine-tuning of PS exposure and MP release in response to a variety of specific stimuli. The pharmacological modulation of MP release may have a substantial therapeutic impact in the management of atherothrombotic vascular disorders. Because PS exposure is a key feature in pathological processes different from hemostasis and thrombosis, the most important obstacle in the field of MP-modulating drugs seems to be carefully targeting MP release to relevant cell types at an optimal level, so as to achieve a beneficial action and limit possible adverse effects. (Arterioscler Thromb Vasc Biol. 2011;31:15-26.)

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“…According to this, one of the possible mechanisms of PS exposure in viral envelope is the increase of cytoplasmic calcium, as observed during HIV‐1, hepatitis C, and YFV infection. Increased calcium concentration activates calcium‐dependent scramblases that exposes PS to the outer plasma membrane. Hence, the viral particle acquires the PS during the budding from cell membrane.…”

Section: Introductionmentioning

confidence: 99%

Viral receptors for flaviviruses: Not only gatekeepers

Oliveira

Peron²

2019

Journal of Leukocyte Biology

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Arboviruses have been a huge threat for human health since the discovery of yellow fever virus in 1901. Arboviruses are arthropod born viruses, mainly transmitted by mosquitoes and ticks, responsible for more than thousands of deaths annually. The Flavivirideae family is probably the most clinically relevant, as it is composed of very important agents, such as dengue, yellow fever, West Nile, Japanese encephalitis, and, recently, Zika virus. Intriguingly, despite their structural and genomic similarities, flaviviruses may cause conditions ranging from mild infections with fever, cutaneous rash, and headache, to very severe cases, such as hemorrhagic fever, encephalitis, Guillain‐Barré syndrome, and microcephaly. These differences may greatly rely on viral burden, tissue tropism, and mechanisms of immune evasion that may depend on both viral and host genetic factors. Unfortunately, very little is known about the biology of these factors, and how they orchestrate these differences. In this context, viral structural proteins and host cellular receptors may have a great relevance, as their interaction dictates not only viral tissue tropism, but also a plethora on intracellular mechanisms that may greatly account for either failure or success of infection. A great number of viral receptors have been described so far, although there is still a huge gap in understanding their overall role during infection. Here we discuss some important aspects triggered after the interaction of flaviviruses and host membrane receptors, and how they change the overall outcome of the infection.

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Effects of divalent cations on lipid flip-flop in the human erythrocyte membrane

Cited by 53 publications

References 40 publications

Protein Involvement in Transmembrane Lipid Asymmetry

Protein Involvement in Transmembrane Lipid Asymmetry

Cellular Mechanisms Underlying the Formation of Circulating Microparticles

Viral receptors for flaviviruses: Not only gatekeepers

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