Topic
Phosphatidylserine
About: Phosphatidylserine is a research topic. Over the lifetime, 4447 publications have been published within this topic receiving 230818 citations. The topic is also known as: distearoylphosphatidylserine & PS.
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TL;DR: The data suggest that macrophages specifically recognize phosphatidylserine that is exposed on the surface of lymphocytes during the development of apoptosis, and suggest that apoptotic lymphocytes lose membrane phospholipid asymmetry and expose phosphorus on the outer leaflet of the plasma membrane.
Abstract: During normal tissue remodeling, macrophages remove unwanted cells, including those that have undergone programmed cell death, or apoptosis. This widespread process extends to the deletion of thymocytes (negative selection), in which cells expressing inappropriate Ag receptors undergo apoptosis, and are phagocytosed by thymic macrophages. Although phagocytosis of effete leukocytes by macrophages has been known since the time of Metchnikoff, only recently has it been recognized that apoptosis leads to surface changes that allow recognition and removal of these cells before they are lysed. Our data suggest that macrophages specifically recognize phosphatidylserine that is exposed on the surface of lymphocytes during the development of apoptosis. Macrophage phagocytosis of apoptotic lymphocytes was inhibited, in a dose-dependent manner, by liposomes containing phosphatidyl-L-serine, but not by liposomes containing other anionic phospholipids, including phosphatidyl-D-serine. Phagocytosis of apoptotic lymphocytes was also inhibited by the L isoforms of compounds structurally related to phosphatidylserine, including glycerophosphorylserine and phosphoserine. The membranes of apoptotic lymphocytes bound increased amounts of merocyanine 540 dye relative to those of normal cells, indicating that their membrane lipids were more loosely packed, consistent with a loss of membrane phospholipid asymmetry. Apoptotic lymphocytes were shown to express phosphatidylserine (PS) externally, because PS on their surfaces was accessible to derivatization by fluorescamine, and because apoptotic cells expressed procoagulant activity. These observations suggest that apoptotic lymphocytes lose membrane phospholipid asymmetry and expose phosphatidylserine on the outer leaflet of the plasma membrane. Macrophages then phagocytose apoptotic lymphocytes after specific recognition of the exposed PS.
3,344 citations
TL;DR: It is shown that PS externalization is an early and widespread event during apoptosis of a variety of murine and human cell types, regardless of the initiating stimulus, and precedes several other events normally associated with this mode of cell death.
Abstract: A critical event during programmed cell death (PCD) appears to be the acquisition of plasma membrane (PM) changes that allows phagocytes to recognize and engulf these cells before they rupture. The majority of PCD seen in higher organisms exhibits strikingly similar morphological features, and this form of PCD has been termed apoptosis. The nature of the PM changes that occur on apoptotic cells remains poorly defined. In this study, we have used a phosphatidylserine (PS)-binding protein (annexin V) as a specific probe to detect redistribution of this phospholipid, which is normally confined to the inner PM leaflet, during apoptosis. Here we show that PS externalization is an early and widespread event during apoptosis of a variety of murine and human cell types, regardless of the initiating stimulus, and precedes several other events normally associated with this mode of cell death. We also report that, under conditions in which the morphological features of apoptosis were prevented (macromolecular synthesis inhibition, overexpression of Bcl-2 or Abl), the appearance of PS on the external leaflet of the PM was similarly prevented. These data are compatible with the notion that activation of an inside-outside PS translocase is an early and widespread event during apoptosis.
2,939 citations
TL;DR: The results indicate that the phase in apoptosis that is characterized by chromatin condensation coincides with phosphatidylserine exposure, which precedes membrane damage that might lead to release from the cells of enzymes that are harmful to the surrounding tissues.
2,465 citations
TL;DR: The basic mechanisms underlying the loss of membrane asymmetry during apoptosis are described and the novel annexin V-binding assay is discussed, an extension to the current available methods.
Abstract: Apoptosis is a programmed, physiological mode of cell death that plays an important role in tissue homeostasis. Understanding of the basic mechanisms that underlie apoptosis will point to potentially new targets of therapeutic treatment of diseases that show an imbalance between cell proliferation and cell loss. In order to conduct such research, techniques and tools to reliably identify and enumerate death by apoptosis are essential. This review focuses on a novel technique to detect apoptosis by targeting for the loss of phospholipid asymmetry of the plasma membrane. It was recently shown that loss of plasma membrane asymmetry is an early event in apoptosis, independent of the cell type, resulting in the exposure of phosphatidylserine (PS) residues at the outer plasma membrane leaflet. Annexin V was shown to interact strongly and specifically with PS and can be used to detect apoptosis by targeting for the loss of plasma membrane asymmetry. Labeled annexin V can be applied both in flow cytometry and in light microscopy in both vital and fixed material by using appropriate protocols. The annexin V method is an extension to the current available methods. This review describes the basic mechanisms underlying the loss of membrane asymmetry during apoptosis and discusses the novel annexin V-binding assay. Cytometry 31:1–9, 1998. © 1998 Wiley-Liss, Inc.
1,848 citations
01 Jan 1980
TL;DR: This research attacked the mode of action of phosphatidylcholine-like deposits in response to the presence of ribonucleic acid by exploiting its role as a “spatially aggregating substance” in the response to EMT.
Abstract: IAbbreviations used in this article are as follows: AraC= l -,B-d arabinofuranosyl cytosine, Chol=cholesterol, DNA=deoxyribonucleic acid, DMPA=dimyristoyl phos phatidic acid, DMPC = dimyristoyl phosphatidylcholine, DMPE = dimyristoyl phos phatidylethanolamine, DOPC = dioleoyl phosphatidylcholine, DOPE = dioleoyl phos phatidylethanolamine, DPPA=dipaJmitoyl phosphatidic acid, DPPC=dipaJmitoyl phos phatidylcholine, DPPG = dipaJmitoyl phosphatidylglycerol, DPPS;= dipalmitoyl phos phatidylserine, DSPC = distearoyl phosphatidylcholine, EPC = egg phosphatidylcholine, EDTA=ethylene diamine tetracetic acid, HDL=high density lipoprotein, HPLC=high performance liquid chromatography, LUV = large unilamellar vesicle, MLV = multilamellar vesicle, NT A = nitrilotriacetic acid, NMR = nuclear magnetic resonance, PA phosphatidic acid, PC = phosphatidylcholine, PE = phosphatidylethanolamine, PO = phosphatidylglycerol, PS = phosphatidylserine, REV = reverse-phase evaporation vesicle, RNA = ribonucleic acid, SUV=small unilameUar vesicle, Tc=transition temperature. 2Present address: Department of Physiology, Tufts University School of Medicine, Boston, Massachusetts 02111.
1,666 citations