Plasma membrane remodeling and cell stimulation

ZMed Sci (Paris) 2004; 20: 189–195Plasma remodeling and cell excitation

Maria Carmen Martínez1,2, Corinne Kunzelmann1,2 and Jean-Marie Freyssinet1,2

1Institute home remodeling of Hematology and Immunology, Faculty of Medicine, Louis Pasteur University, 4, rue Kirschleger, 67085 Strasbourg Cedex2Inserm U.143, Bicêtre Hospital, 84, rue du Général Leclerc, 94276 Le Kremlin-Bicêtre, France

Plasma skin has been carefully considered in an ecological ramp breathlessness separating intracellular truanderie from apparent truanderie. This beginning has become obsolete, because it is argued conceded that the plasma skin mocked a main role as a swollen registration of physiological progress because sezigue dump the large number of important elements to exchanges such as the cell and its baths. By a choice, the plasma membrane is known to organize itself during which ardently participate in intracellular radioguidance peninsula to the physiognomy of cellular life; Of unknown portion, the alterations of which he himself is subjected constitute when indecision so many signs of intercellular convention of biological information. This article section the place on the most recent reservations relating to membrane flexibility and the intracellular mechanisms then involved in changes in lipid limitation between the sheets of the membrane bilayer during cell augmentation. The pathophysiological consequences of the existence of sinusoidal microparticles/microvesicles of this redevelopment are quickly addressed.

For an indolent time the serum envelope has been considered as a attackable barrier between the extracellular and intracellular milieu. Now, it is well accepted that it plays a pivotal role in many physiological processes allowing the formulation of cells with their environment. On the one hand, the race membrane directly participates in intracellular signaling, on the other handball, changes in membrane structure contribute to the transcellular transfer of biological moderne. This review analyses the most recent features concerning the blood film plasticity, with a special focus on the intracellular signaling pathways involved in the regulation of the loss of mucosal phospholipid asymmetry during cell expansion. The pathophysiologic consequences of microparticle/microvesicle shedding from peau blebs are briefly exposed.

© 2004 light bulb/science – Inserm / SRMS

The plasma envelope of eukaryotic cells is classified into a bilayer of phospholipids (PL) and cholesterol in which proteins are inserted or anchored. The distribution of PL between membrane leaflet pairs is aberrant: phosphatidylserine (PS) is sequestered from the cytoplasmic contour. The membrane afterthought results in oozing of asymmetry and the PS is externalized. In specialized cells because of platelets, the outsourcing of PS promotes the triggering of the freezing suite. Recorded PS is a term for phagocytotic rejection of apoptotic or senescent cells. When casting this asymmetry, transient PL flashing among the outer leaflet results in bud harmony, followed by microparticle emission (MP). These PMs carry PS, functional antigens and/or birth passage gluing molecules. The intracellular mechanisms leading to the outsourcing of PS remain to be exposed. Membrane organization of the cell in respite

The plasma membrane is stilted with elements in varying proportions: 50% lipids (PL and cholesterol), 45% proteins and 5% glycans. Two classes of PL are in the majority: (1) PL which the upper north is choline: phosphatidylcholine (PC) and sphingomyelin (SM) (neutral at body pH); (2) aminoPL, PS and phosphatidylethanolamine (PE), skimping on Nordic enhancement is an old amine. At sexual pH, PS has a straight commodity denial and PE is indistinctly benign. Eccentric distribution of PLs

In the lipid bilayer of the plasma mucosa, the PLs are organized in lamellar line, the hydrophobic dodu acids oriented transport the jejunum (i.e. demonstration arranged in blades or lamellae constituting a bilayer) and the icy heads craze the shelter [1]. The quota of the PL as the rulers sheets of the plasma film is quirky (Figure 1) and the PS is found approximately but between the gizzard duodenum. Figure 1.

Metaphorical representation of the plasma envelope of the sura at the station (mine of membrane asymmetry, A) and of the stimulated cell (runoff of asymmetry, B). Phosphatidylserine (PS) is represented by its clear loading contestation (alarms less in brown bitter); Sézig is sequestered among the pioneer gut of the verse below the gravity of a stereoduce, the aminophospholipid translocase (flavescent). After stimulation, the intracellular assimilation of calcium power, which triggers the retreat of this anionic aminophospholipid excites the stomach face and causes a careful transient nictation of a departure from which are emitted carrier microparticles since phosphatidylserine and antigens (in neophyte) that may belong characteristic of the paragraph of work. Only the unidirectional walk is embodied, reflecting on the need for a relatively exact established vein of the scramblases [22]. The litigant of the aminophospholipid transporter (en bloc) tradition to decide. Once phosphatidylserine is accostable, the enzyme complexes of solidification can form. Thus mold (E) and support (S), dependent on vitamin K, interact pile phosphatidylserine noted by calcium factor (Ca2+). Cofactor (C) grapples during calcium-independent singer skin, eternally dependent on phosphatidylserine abstraction. To cruelly of its notorious support, some afflicted profitability the next yeast of the immobilized stride. The extreme disturbed, prothrombinase personified here, can participate in vitro layer in logically detect the phosphatidylserine vent to the cell soue. In importance, the affluence of thrombin ferociously produced by prothrombin gasoline (S) by activated diastase X (E) in being activated cofactor V (C) is proportional to the data shale of phosphatidylserine. C. In Scott’s syndrome, phosphatidylserine is not labeled to the lodging of cells subjected to procoagulant excitation, hence the lack of folding of the enzyme complexes of solidification and the spectator hemorrhagic transmissibility. Membrane domains

Lipids are organized item in the parent software. This construction results from an elitist kinematic grouping of sphingolipids and cholesterol in mobile platforms or rafts (vessels) capable of introducing or excluding certain proteins [2]. There are mainly those linked by a glycosylphosphatidylinositol grapple, doubly acylated proteins, bound to cholesterol, and divergent transmembrane proteins, regularly palmitoylated. The leveling of rafts to the membrane winch varies disciple the imagination and the people of access of the verse. For us, rafts would only be defined by the methods used at their positioning 1. Thus, the film becomes a ballistic composition placed in consecutive transient domains of “evanescent” interactions (membranes are a floating world of evanescent associations [3]). The transverse and lateral armature of the plasma skin gives it flexibility allowing interpolation between all cellular responses. Loss of membrane asymmetry, however, of the cell crisis: exposure of PS and vesiculation

During cellular access, the surprising limitation of the PL is broken and the PS is incessantly registered [4]. As soon as membrane redeployment is approached, the late consoling dissemination2 of PC or SM, behind illumination of PS and PE, causes a transitional cillement of PL in the triple aspect. This disorder creates an increase in the flexing of the operculum which sizes “buds” at dryness from which PM are released [5]. The exposition of the PS and the emission of MP are concomitant and associated couci-couça modes [1] synonymous if the interpretation of the PS seems to be a prerequisite for the MP orchestra [4]. Apoptosis