Arachidonic acid uptake by human platelets is mediated by CD36

A K DuttaRoy, Margaret Jane Gordon, Fiona Margaret Campbell, Lynn Crosbie

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

The involvement of glycoprotein (GP) IV (CD36) in arachidonic acid uptake by human platelets was investigated using an anti-CD36 monoclonal antibody (MAB). The binding of [C-14]arachidonic acid to MAB-treated platelets was significantly reduced compared with untreated platelets, The MAB also inhibited arachidonic acid-induced platelet aggregation and thromboxane Az synthesis in a dose-dependent manner. Preincubation of gel-filtered platelets with the MAB (10 mg/l) inhibited arachidonic acid-induced platelet aggregation by 50% and collagen-induced platelet aggregation by 7-8% and the lag time was increased by 200%, Although the mechanism of platelet aggregation is not fully understood yet, the inhibition of arachidonic acid-induced platelet aggregation by the MAB could be the result of a reduced uptake of exogeneously added arachidonic acid by the MAB-treated platelets, Our data clearly indicate that arachidonic acid uptake by platelets is mediated, at least in part, by CD36.

Original languageEnglish
Pages (from-to)291-295
Number of pages5
JournalPlatelets
Volume7
Issue number5-6
Publication statusPublished - 1996

Keywords

  • GLYCOPROTEIN-IV CD36
  • BINDING PROTEIN
  • ACTIVATION
  • DEFICIENCY
  • RECEPTOR
  • GPIV
  • IDENTIFICATION
  • THROMBOSPONDIN
  • PURIFICATION
  • TRANSFUSION
  • glycoprotein-IV CD36
  • binding protein
  • activation
  • deficiency
  • receptor
  • identification
  • thrombospondin
  • purification
  • transfusion

Cite this

DuttaRoy, A. K., Gordon, M. J., Campbell, F. M., & Crosbie, L. (1996). Arachidonic acid uptake by human platelets is mediated by CD36. Platelets, 7(5-6), 291-295.

Arachidonic acid uptake by human platelets is mediated by CD36. / DuttaRoy, A K ; Gordon, Margaret Jane; Campbell, Fiona Margaret; Crosbie, Lynn.

In: Platelets, Vol. 7, No. 5-6, 1996, p. 291-295.

Research output: Contribution to journalArticle

DuttaRoy, AK, Gordon, MJ, Campbell, FM & Crosbie, L 1996, 'Arachidonic acid uptake by human platelets is mediated by CD36', Platelets, vol. 7, no. 5-6, pp. 291-295.
DuttaRoy AK, Gordon MJ, Campbell FM, Crosbie L. Arachidonic acid uptake by human platelets is mediated by CD36. Platelets. 1996;7(5-6):291-295.
DuttaRoy, A K ; Gordon, Margaret Jane ; Campbell, Fiona Margaret ; Crosbie, Lynn. / Arachidonic acid uptake by human platelets is mediated by CD36. In: Platelets. 1996 ; Vol. 7, No. 5-6. pp. 291-295.
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abstract = "The involvement of glycoprotein (GP) IV (CD36) in arachidonic acid uptake by human platelets was investigated using an anti-CD36 monoclonal antibody (MAB). The binding of [C-14]arachidonic acid to MAB-treated platelets was significantly reduced compared with untreated platelets, The MAB also inhibited arachidonic acid-induced platelet aggregation and thromboxane Az synthesis in a dose-dependent manner. Preincubation of gel-filtered platelets with the MAB (10 mg/l) inhibited arachidonic acid-induced platelet aggregation by 50{\%} and collagen-induced platelet aggregation by 7-8{\%} and the lag time was increased by 200{\%}, Although the mechanism of platelet aggregation is not fully understood yet, the inhibition of arachidonic acid-induced platelet aggregation by the MAB could be the result of a reduced uptake of exogeneously added arachidonic acid by the MAB-treated platelets, Our data clearly indicate that arachidonic acid uptake by platelets is mediated, at least in part, by CD36.",
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AU - DuttaRoy, A K

AU - Gordon, Margaret Jane

AU - Campbell, Fiona Margaret

AU - Crosbie, Lynn

PY - 1996

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N2 - The involvement of glycoprotein (GP) IV (CD36) in arachidonic acid uptake by human platelets was investigated using an anti-CD36 monoclonal antibody (MAB). The binding of [C-14]arachidonic acid to MAB-treated platelets was significantly reduced compared with untreated platelets, The MAB also inhibited arachidonic acid-induced platelet aggregation and thromboxane Az synthesis in a dose-dependent manner. Preincubation of gel-filtered platelets with the MAB (10 mg/l) inhibited arachidonic acid-induced platelet aggregation by 50% and collagen-induced platelet aggregation by 7-8% and the lag time was increased by 200%, Although the mechanism of platelet aggregation is not fully understood yet, the inhibition of arachidonic acid-induced platelet aggregation by the MAB could be the result of a reduced uptake of exogeneously added arachidonic acid by the MAB-treated platelets, Our data clearly indicate that arachidonic acid uptake by platelets is mediated, at least in part, by CD36.

AB - The involvement of glycoprotein (GP) IV (CD36) in arachidonic acid uptake by human platelets was investigated using an anti-CD36 monoclonal antibody (MAB). The binding of [C-14]arachidonic acid to MAB-treated platelets was significantly reduced compared with untreated platelets, The MAB also inhibited arachidonic acid-induced platelet aggregation and thromboxane Az synthesis in a dose-dependent manner. Preincubation of gel-filtered platelets with the MAB (10 mg/l) inhibited arachidonic acid-induced platelet aggregation by 50% and collagen-induced platelet aggregation by 7-8% and the lag time was increased by 200%, Although the mechanism of platelet aggregation is not fully understood yet, the inhibition of arachidonic acid-induced platelet aggregation by the MAB could be the result of a reduced uptake of exogeneously added arachidonic acid by the MAB-treated platelets, Our data clearly indicate that arachidonic acid uptake by platelets is mediated, at least in part, by CD36.

KW - GLYCOPROTEIN-IV CD36

KW - BINDING PROTEIN

KW - ACTIVATION

KW - DEFICIENCY

KW - RECEPTOR

KW - GPIV

KW - IDENTIFICATION

KW - THROMBOSPONDIN

KW - PURIFICATION

KW - TRANSFUSION

KW - glycoprotein-IV CD36

KW - binding protein

KW - activation

KW - deficiency

KW - receptor

KW - identification

KW - thrombospondin

KW - purification

KW - transfusion

M3 - Article

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JO - Platelets

JF - Platelets

SN - 0953-7104

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ER -