Abstract
We found that intracellular Ca2+ concentration ([Ca2+](i)) increased during ristocetin-induced agglutination of aequorin loaded platelets resuspended in plasma. Chelation of extracellular Ca2+ had no effect on platelet clumping, but delayed and greatly reduced Ca2+ increase, indicating that it derived for the most part from Ca2+ influx. Nine monoclonal antibodies (MA) against glycoprotein (GP) Ib largely prevented ristocetin-induced platelet clumping and [Ca2+](i) increase, while three anti-GPIb MA with no effect on platelet clumping did not interfere with Ca2+ movement. In unstirred samples platelet agglutination was greatly reduced and [Ca2+](i) increase was abolished, suggesting that close platelet-to-platelet contact in addition to von Willebrand factor (vWF) binding to GPIb, is necessary for Ca2+ transient. Nine MA against GPIIb/IIIa, the gly-arg-gly-asp-ser (GRGDS) peptide and GPIIb/IIIa complex dissociation had no effect on platelet agglutination, but significantly reduced Ca2+ increase. Our results suggest that platelet clumping induced by vWF binding to GPIb is responsible for GPIIb-IIIa dependent Ca2+ influx.
| Original language | English |
|---|---|
| Pages (from-to) | 689-692 |
| Number of pages | 4 |
| Journal | Thrombosis and Haemostasis |
| Volume | 73 |
| Issue number | 4 |
| Publication status | Published - 1995 |
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ASJC Scopus subject areas
- Hematology
Cite this
Ristocetin-induced platelet agglutination stimulates GPIIb/IIIa-dependent calcium influx. / Bertolino, G.; Noris, P.; Spedini, P.; Balduini, C. L.
In: Thrombosis and Haemostasis, Vol. 73, No. 4, 1995, p. 689-692.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Ristocetin-induced platelet agglutination stimulates GPIIb/IIIa-dependent calcium influx
AU - Bertolino, G.
AU - Noris, P.
AU - Spedini, P.
AU - Balduini, C. L.
PY - 1995
Y1 - 1995
N2 - We found that intracellular Ca2+ concentration ([Ca2+](i)) increased during ristocetin-induced agglutination of aequorin loaded platelets resuspended in plasma. Chelation of extracellular Ca2+ had no effect on platelet clumping, but delayed and greatly reduced Ca2+ increase, indicating that it derived for the most part from Ca2+ influx. Nine monoclonal antibodies (MA) against glycoprotein (GP) Ib largely prevented ristocetin-induced platelet clumping and [Ca2+](i) increase, while three anti-GPIb MA with no effect on platelet clumping did not interfere with Ca2+ movement. In unstirred samples platelet agglutination was greatly reduced and [Ca2+](i) increase was abolished, suggesting that close platelet-to-platelet contact in addition to von Willebrand factor (vWF) binding to GPIb, is necessary for Ca2+ transient. Nine MA against GPIIb/IIIa, the gly-arg-gly-asp-ser (GRGDS) peptide and GPIIb/IIIa complex dissociation had no effect on platelet agglutination, but significantly reduced Ca2+ increase. Our results suggest that platelet clumping induced by vWF binding to GPIb is responsible for GPIIb-IIIa dependent Ca2+ influx.
AB - We found that intracellular Ca2+ concentration ([Ca2+](i)) increased during ristocetin-induced agglutination of aequorin loaded platelets resuspended in plasma. Chelation of extracellular Ca2+ had no effect on platelet clumping, but delayed and greatly reduced Ca2+ increase, indicating that it derived for the most part from Ca2+ influx. Nine monoclonal antibodies (MA) against glycoprotein (GP) Ib largely prevented ristocetin-induced platelet clumping and [Ca2+](i) increase, while three anti-GPIb MA with no effect on platelet clumping did not interfere with Ca2+ movement. In unstirred samples platelet agglutination was greatly reduced and [Ca2+](i) increase was abolished, suggesting that close platelet-to-platelet contact in addition to von Willebrand factor (vWF) binding to GPIb, is necessary for Ca2+ transient. Nine MA against GPIIb/IIIa, the gly-arg-gly-asp-ser (GRGDS) peptide and GPIIb/IIIa complex dissociation had no effect on platelet agglutination, but significantly reduced Ca2+ increase. Our results suggest that platelet clumping induced by vWF binding to GPIb is responsible for GPIIb-IIIa dependent Ca2+ influx.
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UR - http://www.scopus.com/inward/citedby.url?scp=0028921269&partnerID=8YFLogxK
M3 - Article
C2 - 7495080
AN - SCOPUS:0028921269
VL - 73
SP - 689
EP - 692
JO - Thrombosis and Haemostasis
JF - Thrombosis and Haemostasis
SN - 0340-6245
IS - 4
ER -