Expression of phosphatidylserine (PS) on wild-type and Gerbich variant erythrocytes following glycophorin-C (GPC) ligation

被引:32
作者
Head, DJ
Lee, ZE
Poole, J
Avent, ND
机构
[1] Univ W England, Biomed Res Ctr, Bristol BS16 1QY, Frenchay, England
[2] Univ W England, Gen Res Inst, Bristol BS16 1QY, Frenchay, England
[3] Int Blood Grp Reference Lab, Bristol, Frenchay, England
关键词
erythrocyte; glycophorin-C; phosphatidylserine; Gerbich variants;
D O I
10.1111/j.1365-2141.2005.05407.x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
and is a receptor for the malarial parasite Plasmodium falciparum to invade these cells. A link between GPC binding (ligation) and phosphatidylserine (PS) expression on erythrocytes has been suggested by its appearance on P. falciparum-infected erythrocytes. Phosphatidylserine expression has also been shown to be a marker of cellular death in a number of biological pathways including some in erythrocytes. Using Annexin V binding, we demonstrated that ligation of GPC with mouse mAb (BRIC-10) induced PS expression on normal erythrocytes. Phosphatidylserine exposure was prevented following tryptic digestion of intact erythrocytes. In addition, GPC variant phenotypes Yus (Delta exon 2) and Gerbich (Delta exon 3), which express a truncated extracellular domain, did not express PS following BRIC-10 binding, whereas PS was exposed on Ls(a) erythrocytes (duplication of exon 3). GPC ligation was also shown to result in a concomitant loss of erythrocyte viability in wild-type erythrocytes after 24 h in vitro. These results identify a potential pathway linking GPC to PS exposure on erythrocytes that may have a role in regulating red cell turnover. Further characterization of this pathway may also identify new targets for the treatment of P. falciparum malaria.
引用
收藏
页码:130 / 137
页数:8
相关论文
共 36 条
[1]   2 INDIVIDUALS WITH ELLIPTOCYTIC RED-CELLS APPARENTLY LACK 3 MINOR ERYTHROCYTE-MEMBRANE SIALOGLYCOPROTEINS [J].
ANSTEE, DJ ;
PARSONS, SF ;
RIDGWELL, K ;
TANNER, MJA ;
MERRY, AH ;
THOMSON, EE ;
JUDSON, PA ;
JOHNSON, P ;
BATES, S ;
FRASER, ID .
BIOCHEMICAL JOURNAL, 1984, 218 (02) :615-619
[2]  
ANSTEE DJ, 1991, IMMUNOLOGY, V74, P197
[3]   Immunochemical analysis of the human erythrocyte Rh polypeptides [J].
Avent, ND ;
Liu, W ;
Warner, KM ;
Mawby, WJ ;
Jones, JW ;
Ridgwell, K ;
Tanner, MJA .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1996, 271 (24) :14233-14239
[4]   Human mature red blood cells express caspase-3 and caspase-8, but are devoid of mitochondrial regulators of apoptosis [J].
Berg, CP ;
Engels, IH ;
Rothbart, A ;
Lauber, K ;
Renz, A ;
Schlosser, SF ;
Schulze-Osthoff, K ;
Wesselborg, S .
CELL DEATH AND DIFFERENTIATION, 2001, 8 (12) :1197-1206
[5]   Programmed cell death in mature erythrocytes: a model for investigating death effector pathways operating in the absence of mitochondria [J].
Bratosin, D ;
Estaquier, J ;
Petit, F ;
Arnoult, D ;
Quatannens, B ;
Tissier, JP ;
Slomianny, C ;
Sartiaux, C ;
Alonso, C ;
Huart, JJ ;
Montreuil, J ;
Ameisen, JC .
CELL DEATH AND DIFFERENTIATION, 2001, 8 (12) :1143-1156
[6]  
CATRON JP, 1995, TRANSFUS CLIN BIOL, V2, P251
[7]  
CHANG S, 1991, BLOOD, V77, P644
[8]   Distinct modes of macrophage recognition for apoptotic and necrotic cells are not specified exclusively by phosphatidylserine exposure [J].
Cocco, RE ;
Ucker, DS .
MOLECULAR BIOLOGY OF THE CELL, 2001, 12 (04) :919-930
[9]   IDENTIFICATION OF THE PROTEIN 4.1 BINDING-SITE TO PHOSPHATIDYLSERINE VESICLES [J].
COHEN, AM ;
LIU, SC ;
LAWLER, J ;
DERICK, L ;
PALEK, J .
BIOCHEMISTRY, 1988, 27 (02) :614-619
[10]  
COLIN Y, 1986, J BIOL CHEM, V261, P229