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Mechanism and function of changes in membrane-phospholipid asymmetry in platelets and erythrocytes.

Introduction In the two decades since it was first proposed by Hretscher [ 11, ample evidence has accumulated to support the general view that both leaflets of the lipid bilayer of most, if not all, biological membranes have distinctly different lipid compositions (see [2] for a recent review). Whereas the outer leaflet is generally rich in cholinephospholipids, sphingomyelin and phosphatidylcholine, the inner leaflet is preferentially occupied by aminophospholipids, phosphatidylethanolamine and phosphatidylserine. Despite the fact that membrane-phospholipid asymmetry has become widely appreciated as a ubiquitous phenomenon, the mechanisms involved in its regulation and maintenance have begun to be addressed only recently. The discovery of an ATP-dependent aminophospholipid-specific transporter, which shuttles phosphatidylserine and phosphatidylethanolamine across the bilayer membrane towards the inner leaflet [3], suggests that a specific transmembrane orientation of these lipids is of major importance for cell function. Although our understanding of the physiological role of membrane lipid asymmetry is still fragmentary, there is evidence to suggest that exposure of phosphatidylserine at the cell surface which can occur during cell activation provides a signal for cell-cell recognition [4, 51 and is instrumental in promoting blood coagulation [6,7]. In this article we address the possible mechanisms which may play a role in the loss of membrane-phospholipid asymmetry that happens upon activation of blood platelets or upon CaZ+entry into red blood cells. In addition we will highlight an experiment of nature by featuring a rare bleeding disorder in which these phenomena do not occur.