In keratinocytes, osteoclasts and enterocytes, Ni2+ acts as an agonist working through selective activation of the polyvalent cation-sensing receptor. We report here that while Ni2+ alone had no direct ability to induce platelet aggregation or secretion, Ni2+ pretreatment produced these responses when platelets were stimulated with subthreshold concentrations of collagen. In addition, pretreatment with Ni2+ significantly enhanced collagen-induced phospholipase C activation and calcium mobilization. Platelet adhesion to collagen was increased and the inhibition of collagen-induced adhesion normally seen after cytochalasin D treatment was significantly diminished. When Ni2+ was added to platelets alone, tyrosine phosphorylation of p60(src) was increased. Moreover, Ni2+ enhanced the amount of protein, especially actin, found in the low-speed Triton X-100 insoluble cytoskeleton. Our results indicate that nickel, possibly acting via a platelet cation sensing receptor analogous to that which has been described in other cell types, may cause a rapid tyrosine kinase-dependent cytoskeleton reorganization leading to enhanced adhesion of platelets to collagen and increasing collagen-dependent responses.

Nickel enhances collagen-induced platelet activation acting by increasing the organization of the cytoskeleton / Pulcinelli, FABIO MARIA; S., Sebastiani; M., Pesciotti; Pignatelli, Pasquale; Gazzaniga, Pierpaolo; Daniel, Jl. - In: THROMBOSIS AND HAEMOSTASIS. - ISSN 0340-6245. - 79:2(1998), pp. 395-399.

Nickel enhances collagen-induced platelet activation acting by increasing the organization of the cytoskeleton

PULCINELLI, FABIO MARIA;PIGNATELLI, Pasquale;GAZZANIGA, Pierpaolo;
1998

Abstract

In keratinocytes, osteoclasts and enterocytes, Ni2+ acts as an agonist working through selective activation of the polyvalent cation-sensing receptor. We report here that while Ni2+ alone had no direct ability to induce platelet aggregation or secretion, Ni2+ pretreatment produced these responses when platelets were stimulated with subthreshold concentrations of collagen. In addition, pretreatment with Ni2+ significantly enhanced collagen-induced phospholipase C activation and calcium mobilization. Platelet adhesion to collagen was increased and the inhibition of collagen-induced adhesion normally seen after cytochalasin D treatment was significantly diminished. When Ni2+ was added to platelets alone, tyrosine phosphorylation of p60(src) was increased. Moreover, Ni2+ enhanced the amount of protein, especially actin, found in the low-speed Triton X-100 insoluble cytoskeleton. Our results indicate that nickel, possibly acting via a platelet cation sensing receptor analogous to that which has been described in other cell types, may cause a rapid tyrosine kinase-dependent cytoskeleton reorganization leading to enhanced adhesion of platelets to collagen and increasing collagen-dependent responses.
1998
01 Pubblicazione su rivista::01a Articolo in rivista
Nickel enhances collagen-induced platelet activation acting by increasing the organization of the cytoskeleton / Pulcinelli, FABIO MARIA; S., Sebastiani; M., Pesciotti; Pignatelli, Pasquale; Gazzaniga, Pierpaolo; Daniel, Jl. - In: THROMBOSIS AND HAEMOSTASIS. - ISSN 0340-6245. - 79:2(1998), pp. 395-399.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/244450
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