1986
DOI: 10.1111/j.1432-1033.1986.tb09833.x
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Expression of intracellular fibrinogen on the surface of stimulated platelets

Abstract: Participation of fibrinogen in platelet aggregation is contingent upon the capacity of various stimuli to induce specific receptors for the molecule on the surface of the cell. The interaction of fibrinogen with this receptor results directly in platelet aggregation, and dissociation of fibrinogen is associated with disaggregation. While the role of exogenous fibrinogen in this process has been fully documented, the mechanisms which control the surface exposure of platelet fibrinogen are less understood. In th… Show more

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Cited by 35 publications
(14 citation statements)
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References 26 publications
(5 reference statements)
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“…However, although inhibiting by more than 85% the binding of '251-fibrinogen to platelets, AP-2 does not prevent the surface expression of platelet fibrinogen upon thrombin stimulation (Legrand, C., unpublished results). A similar finding for platelet fibrinogen has also been observed by Courtois et al [43] using another antibody to GPIIb-IIIa complexes. Thus, these results do not preclude the possibility that thrombospondin is expressed through an interaction with fibrinogen bound to GPIIb-IIIa complexes at an early stage of the secretion process.…”
Section: Discussionsupporting
confidence: 87%
“…However, although inhibiting by more than 85% the binding of '251-fibrinogen to platelets, AP-2 does not prevent the surface expression of platelet fibrinogen upon thrombin stimulation (Legrand, C., unpublished results). A similar finding for platelet fibrinogen has also been observed by Courtois et al [43] using another antibody to GPIIb-IIIa complexes. Thus, these results do not preclude the possibility that thrombospondin is expressed through an interaction with fibrinogen bound to GPIIb-IIIa complexes at an early stage of the secretion process.…”
Section: Discussionsupporting
confidence: 87%
“…Interestingly, the reduction in IAC-1 binding to ␣ 2 ␤ 1 on CVX-stimulated platelets in plasma where ␣ IIb ␤ 3 is blocked by aggrastat ( Figure 4A) was notably lower than the observed IAC-1 binding to ␣ 2 ␤ 1 on CVX-stimulated washed platelets ( Figure 1A). This suggests that autocrine fibrinogen, present in platelet ␣-granules (about 1 mg fibrinogen/10 10 platelets) and released upon platelet activation, 41 contributes to ␣ IIb ␤ 3 -mediated IAC-1 binding to washed platelets.…”
Section: Org Frommentioning
confidence: 99%
“…Platelet aggregation is provoked by the appearance on the cell surface of new proteins [2] and/or new phospholipids [3]. These factors come from plasma (coagulation factors [4], fibrinogen [5]) or from within the platelets (fibrinogen [6], different coagulation factors [7,8], phosphatidylserine [9]) depending on the organism. The present study demonstrates that a protein very similar to serum albumin is released from rabbit platelets under the influence of platelet activating factor (PAF-acether), with some evidence of a small contribution from cellular granules.…”
Section: Platelet-activating-factor-induced Serum-albumin Release Fromentioning
confidence: 99%