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Query: UMLS:C0344329 (collapse)
 28,634 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Reports on non-neural cells have shown that enhanced activity of the Ca(2+)-dependent/ATP-independent phospholipid scramblase (PLSCR1) is, at least in part, responsible for surface exposure of phosphatidylserine and the collapse of plasma membrane asymmetry in injured or apoptotic cells. To shed some light on mechanisms with a potential to lead to apoptotic death of human neurones following ischemic/hypoxic injury, we examined the immunoreactivity of hippocampal neurones for PLSCR1, caspase-3, cytochrome c and DNA-fragmentation in 22 individuals with clinically symptomatic cerebral ischemia after cardiac arrest or severe hypotension. WE FOUND: (1) significant differences in the percentage of PLSCR1-immunoreactive neurones between controls and short survivors; statistically strong differences between the frequency of immunoreactive neurones among the subfields studied with lowest levels in the CA3; preferential distribution of immunoreactive neurones in controls within the regio entorhinalis, subfield CA1, and hilum. Additionally, these areas exhibited staining of fibre bundles which probably correspond to perforant path, alvear path and collateral's of Schaffer, (2) caspase-3 was upregulated in a region-specific manner with marked activation in the selectively vulnerable hippocampal areas, (3) cytochrome c was redistributed, (4) DNA-fragmentation represented by scattered TUNEL-positive cells increased predominantly during the first 3 days after ischemia, and particularly in the regions of greatest susceptibility to hypoxic injury. This study presents the first evidence that PLSCR1, and probably remodelling of plasma membrane phospholipids (PL), plays a role in ischemic injury in the human hippocampus.
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PMID:Spatial resolution of phospholipid scramblase 1 (PLSCR1), caspase-3 activation and DNA-fragmentation in the human hippocampus after cerebral ischemia. 1260 85

During capacitation, major changes take place in the sperm plasma membrane so as to render it fusogenic and responsive to zona pellucida glycoproteins. However, the mechanisms involved have not been defined. As bicarbonate is known to be the key component that induces capacitation, we have investigated the bicarbonate-dependent changes in the boar sperm's plasma membrane architecture. We have discovered that bicarbonate induces a rapid collapse of phospholipid transverse asymmetry, exposing phosphatidylethanolamine and phosphatidylserine at the outer surface of the lipid bilayer. The collapse, which is reversible, is brought about as a result of activation of the phospholipid scramblase that exchanges phospholipids in a non-specific fashion between the two leaflets of the lipid bilayer. The activation takes place via a cyclic AMP-protein kinase A-dependent pathway and is initiated via stimulation of the so-called 'soluble' adenylyl cyclase in the sperm cell by bicarbonate. As a result of the collapse and the concurrent increase in phospholipid exchange, removal of cholesterol by albumin is facilitated (perhaps due to increased lipid packing disorder). This finding is in conflict with earlier surmises that cholesterol loss precedes activation of the cyclic AMP-protein kinase A axis. We have noted that not all cells in a given sperm population show rapid changes in response to bicarbonate stimulation; samples from individual boars also differ in their response. Maturation differences between cells have been found to play an important role in such functional heterogeneity.
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PMID:Bicarbonate-induced membrane processing in sperm capacitation. 1562 3

The best understood consequence of the collapse of lipid asymmetry is exposure of phosphatidylserine (PS) in the external leaflet of the plasma membrane bilayer, where it is known to serve at least two major functions: providing a platform for development of the blood coagulation cascade and presenting the signal that induces phagocytosis of apoptotic cells. Lipid asymmetry is collapsed by activation of phospholipid scramblase(s) that catalyze bidirectional transbilayer movement of the major classes of phospholipid. The protein corresponding to this activity is not yet known. Observations on cells from patients with Scott syndrome, a rare hereditary bleeding disorder resulting from impaired lipid scrambling, have shown that there are multiple activation pathways that converge on scramblase activity.
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PMID:Phospholipid scramblase: an update. 2030 64

Calcium-activated phospholipid scramblase mediates the energy-independent bidirectional translocation of lipids across the bilayer, leading to transient or, in the case of apoptotic scrambling, sustained collapse of membrane asymmetry. Cells lacking TMEM16F-dependent lipid scrambling activity are deficient in generation of extracellular vesicles (EVs) that shed from the plasma membrane in a Ca2+-dependent manner, namely microvesicles. We have adapted chemical induction of giant plasma membrane vesicles (GPMVs), which require both TMEM16F-dependent phospholipid scrambling and calcium influx, as a kinetic assay to investigate the mechanism of TMEM16F activity. Using the GPMV assay, we identify and characterize both inactivating and activating mutants that elucidate the mechanism for TMEM16F activation and facilitate further investigation of TMEM16F-mediated lipid translocation and its role in extracellular vesiculation.
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PMID:Chemically induced vesiculation as a platform for studying TMEM16F activity. 3062 79