Deciphering the plasma membrane hallmarks of apoptotic cells: Phosphatidylserine transverse redistribution and calcium entry

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Deciphering the plasma membrane hallmarks of apoptotic cells: Phosphatidylserine transverse redistribution and calcium entry

Publisher
BioMed Central
Publication Date
Oct 17, 2001
Source
PMC
Keywords
Disciplines
  • Biology
License
Unknown

Abstract

1471-2121-2-20.fm ral BioMed CentBMC Cell Biology BMC Cell Biology 2001, 2 :20Research article Deciphering the plasma membrane hallmarks of apoptotic cells: Phosphatidylserine transverse redistribution and calcium entry M Carmen Martínez1,2 and Jean-Marie Freyssinet*1,2 Address: 1Institut d'Hématologie et d'Immunologie, Faculté de Médecine, Université Louis Pasteur, 4, rue Kirschleger, 67085, Strasbourg, France and 2Unité 143 INSERM, Hôpital de Bicêtre, 94276, Le Kremlin-Bicêtre, France E-mail: M Carmen Martínez - [email protected]; Jean-Marie Freyssinet* - [email protected] strasbg.fr *Corresponding author Abstract Background: During apoptosis, Ca2+-dependent events participate in the regulation of intracellular and morphological changes including phosphatidylserine exposure in the exoplasmic leaflet of the cell plasma membrane. The occurrence of phosphatidylserine at the surface of specialized cells, such as platelets, is also essential for the assembly of the enzyme complexes of the blood coagulation cascade, as demonstrated by hemorrhages in Scott syndrome, an extremely rare genetic deficiency of phosphatidylserine externalization, without other apparent pathophysiologic consequences. We have recently reported a reduced capacitative Ca2+ entry in Scott cells which may be part of the Scott phenotype. Results: Taking advantage of these mutant lymphoblastoid B cells, we have studied the relationship between this mode of Ca2+ entry and phosphatidylserine redistribution during apoptosis. Ca2+ ionophore induced apoptosis in Scott but not in control cells. However, inhibition of store- operated Ca2+ channels led to caspase-independent DNA fragmentation and decrease of mitochondrial membrane potential in both control and Scott cells. Inhibition of cytochrome P450 also reduced capacitative Ca2+ entry and induced apoptosis at comparable extents in control and Scott cells. During the apoptotic process, both control and more markedly Scott ce

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