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Titolo:
Intracellular trafficking of the alpha(IIb)beta(3) receptor antagonist, abciximab, in normal and Glanzmann's disease megakaryocytes
Autore:
Masse, JM; Perlemuter, K; Debili, N; Letestu, R; Castaigne, A; Cramer, EM;
Indirizzi:
Hop Henri Mondor, INSERM, U474, F-94010 Creteil, France Hop Henri Mondor Creteil France F-94010 M, U474, F-94010 Creteil, France Inst Gustave Roussy, INSERM, U362, F-94805 Villejuif, France Inst Gustave Roussy Villejuif France F-94805 , F-94805 Villejuif, France Hop Henri Mondor, Federat Cardiol, F-94010 Creteil, France Hop Henri Mondor Creteil France F-94010 Cardiol, F-94010 Creteil, France
Titolo Testata:
BRITISH JOURNAL OF HAEMATOLOGY
fascicolo: 4, volume: 107, anno: 1999,
pagine: 720 - 730
SICI:
0007-1048(199912)107:4<720:ITOTAR>2.0.ZU;2-G
Fonte:
ISI
Lingua:
ENG
Soggetto:
GLYCOPROTEIN-IIB-IIIA; MURINE MONOCLONAL-ANTIBODY; GUINEA-PIG MEGAKARYOCYTE; PLATELET ALPHA-GRANULES; IMMUNOGLOBULIN-G; MPL-LIGAND; FIBRINOGEN; FAB; ENDOCYTOSIS; EXPRESSION;
Keywords:
abciximab; alpha(IIb)beta(3); megakaryocytes; platelet inhibitors;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
34
Recensione:
Indirizzi per estratti:
Indirizzo: Cramer, EM Hop Henri Mondor, INSERM, U474, 51 Av MI Lattre de Tassigny, F-94010 Creteil, France Hop Henri Mondor 51 Av MI Lattre de Tassigny CreteilFrance F-94010
Citazione:
J.M. Masse et al., "Intracellular trafficking of the alpha(IIb)beta(3) receptor antagonist, abciximab, in normal and Glanzmann's disease megakaryocytes", BR J HAEM, 107(4), 1999, pp. 720-730

Abstract

The alpha(IIb)beta(3) platelet receptor antagonist abciximab (c7E3Fab, ReoPro(R)) has proved to be effective in preventing arterial thrombosis. However, its binding capacity to the platelet precursors, megakaryocytes (MKs), which also express alpha(IIb)beta(3), is not known, The purpose of this study was to establish whether abciximab is able to react with alpha(IIb)beta(3) located on human MKs, and to follow its subsequent intracellular trafficking. MKs were grown from CD34(+) progenitors from normal subjects and froma patient with type I Glanzmann's thrombasthenia, and abciximab was added at day 10 of culture (4 mu g/ml). Cells were fixed at day 12, cryosectioned, and immunolabelled for abciximab, Labelling was prominent on the MK plasma membrane: it also lined the demarcation membration system. Interestingly,alpha-granule membranes were labelled showing that the antibody was internalized and further stored into MK secretory granules. Abciximab was also strongly detected on and in newly-formed platelets. Glanzmann's disease MKs (which completely lacked alpha(IIb)beta(3)) were consistently negative, confirming that the antibody; fragment was specifically interacting with alpha(IIb)beta(3). In conclusion, this study demon; strated that abciximab: (i) binds MK plasma membrane and demarcation membranes, (ii) trafficks into alpha-granules, and (iii) is expressed on and in nascent platelets. These findings could be taken in account when monitoring anti-alpha(IIb)beta(3) receptor therapy.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/09/20 alle ore 15:36:49