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Decreased Arachidonic Acid Metabolism in Human Platelets by Autologous Neutrophils: Possible Role of Cell Adhesion

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Journal Biochem J
Specialty Biochemistry
Date 1994 Jun 15
PMID 7516654
Citations 1
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Abstract

The amount of the 12-lipoxygenase and cyclo-oxygenase products, 12(S)-hydroxy-(Z,Z,E,Z)-5,8,10,14-eicosatetraenoic acid (12-HETE) and 12(S)-hydroxy-(E,E,Z)-5,8,10-heptadecatrienoic acid (HHT), in human platelets stimulated by thrombin (0.1 and 2.5 units/ml), was studied in the presence of autologous neutrophils. A decreased formation of both products was induced by unstimulated neutrophils or neutrophils challenged with N-formylmethionyl- leucyl-phenylalanine (0.1 microM) or Ca2+ ionophore A23187 (0.15 microM). The effect of neutrophils was observed only in the presence of Ca2+. 12-HETE and HHT were also produced in platelets stimulated with thrombin in the absence of Ca2+ and/or Mg2+, but their level was not altered by neutrophils. 12(S),20-Dihydroxy-(Z,Z,E,Z)-5,8,10,14-eicosatetraenoic acid (12,20-DHETE), the cytochrome P-450 product from 12-HETE in neutrophils, was hardly detected, and its level did not compensate for the decrease in 12-HETE observed after platelet and neutrophil co-incubation. 5(S),12(S)-Dihydroxy-(E,Z,E,Z)- 6,8,10,14-eicosatetraenoic acid (5(S),12(S)-DHETE), the 5-lipoxygenase product of 12-HETE in neutrophils, was never detectable. In addition, the inhibition of 12-HETE and HHT formations appeared not to be due to degradation or thrombin uptake by neutrophils, nor was the decrease observed when the two cell populations were physically separated. A monoclonal antibody against the human platelet glycoprotein GMP140 (CD62), mediating Ca(2+)-dependent platelet-neutrophil adhesion, mimicked the inhibitory effect of neutrophils in a dose-dependent fashion. Furthermore, the 12-HETE and HHT productions were not affected when platelets were stimulated in the presence of neutrophils previously incubated with sialidase, which removes the sialic acid from a sialyl Lewis(x) structure assumed to be the neutrophil receptor for platelet GMP140. We conclude that the decrease in thrombin-stimulated 12-HETE and HHT formation observed when platelets were co-incubated with autologous neutrophils might be the consequence of platelet-neutrophil adherence, presumably through platelet GMP140.

Citing Articles

Adhesion of platelets to chemotactically responsive and non-responsive neutrophils.

Pastakia K, Brownson N, Terle D, Harvath L Clin Mol Pathol. 1996; 49(1):M17-22.

PMID: 16696039 PMC: 408012. DOI: 10.1136/mp.49.1.m17.

References
1.
Pace-Asciak C, Klein J, Spielberg S . Metabolism of leukotriene A4 into C4 by human platelets. Biochim Biophys Acta. 1986; 877(1):68-74. DOI: 10.1016/0005-2760(86)90119-0. View

2.
Antoine C, Murphy R, Henson P, Maclouf J . Time-dependent utilization of platelet arachidonic acid by the neutrophil in formation of 5-lipoxygenase products in platelet-neutrophil co-incubations. Biochim Biophys Acta. 1992; 1128(2-3):139-46. DOI: 10.1016/0005-2760(92)90299-b. View

3.
Robertson D, Page C . Effect of platelet agonists on airway reactivity and intrathoracic platelet accumulation. Br J Pharmacol. 1987; 92(1):105-11. PMC: 1853636. DOI: 10.1111/j.1476-5381.1987.tb11301.x. View

4.
Maclouf J, Murphy R . Transcellular metabolism of neutrophil-derived leukotriene A4 by human platelets. A potential cellular source of leukotriene C4. J Biol Chem. 1988; 263(1):174-81. View

5.
Lagarde M, Gualde N, Rigaud M . Metabolic interactions between eicosanoids in blood and vascular cells. Biochem J. 1989; 257(2):313-20. PMC: 1135582. DOI: 10.1042/bj2570313. View