The antiplatelet activity of Escherichia coli lipopolysaccharide is mediated through a nitric oxide/cyclic GMP pathway

Joen Rong Sheu, W. C. Hung, Ching-Hua Su, C. H. Lin, L. W. Lee, Y. M. Lee, M. H. Yen

Research output: Contribution to journalArticle

22 Citations (Scopus)

Abstract

In this study, Escherichia coli LPS dose-dependently (100-500 μg/ml) and time-dependently (10-60 min) inhibited platelet aggregation in human and rabbit platelets stimulated by agonists. LPS also dose-dependently inhibited the intracellular Ca mobilization in human platelets stimulated by collagen. In addition, LPS (200 and 500 μg/ml) significantly increased the formation of cyclic GMP but not cyclic AMP in platelets. LPS (200 μg/ml) significantly increased the production of nitrate within a 10-min incubation period. Furthermore, LPS also dose-dependently inhibited platelet aggregation induced by PDBu (30 nmol/1), a protein kinase C activator. These results indicate that the antiplatelet activity of E. coli LPS may be involved in the activation of a nitric oxide/cyclic GMP pathway in platelets, resulting in inhibition of platelet aggregation. Therefore, LPS-mediated alteration of platelet function may contribute to bleeding diathesis in septicemic and endotoxemic patients.

Original languageEnglish
Pages (from-to)317-326
Number of pages10
JournalEuropean Journal of Haematology
Volume62
Issue number5
Publication statusPublished - 1999

Fingerprint

Cyclic GMP
Lipopolysaccharides
Nitric Oxide
Blood Platelets
Escherichia coli
Platelet Aggregation
Disease Susceptibility
Cyclic AMP
Nitrates
Protein Kinase C
Collagen
Hemorrhage
Rabbits

Keywords

  • Cyclic-GMP
  • Intracellular calcium mobilization
  • LPS
  • Nitric oxide
  • Platelet aggregation

ASJC Scopus subject areas

  • Hematology

Cite this

The antiplatelet activity of Escherichia coli lipopolysaccharide is mediated through a nitric oxide/cyclic GMP pathway. / Sheu, Joen Rong; Hung, W. C.; Su, Ching-Hua; Lin, C. H.; Lee, L. W.; Lee, Y. M.; Yen, M. H.

In: European Journal of Haematology, Vol. 62, No. 5, 1999, p. 317-326.

Research output: Contribution to journalArticle

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AU - Lee, L. W.

AU - Lee, Y. M.

AU - Yen, M. H.

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AB - In this study, Escherichia coli LPS dose-dependently (100-500 μg/ml) and time-dependently (10-60 min) inhibited platelet aggregation in human and rabbit platelets stimulated by agonists. LPS also dose-dependently inhibited the intracellular Ca mobilization in human platelets stimulated by collagen. In addition, LPS (200 and 500 μg/ml) significantly increased the formation of cyclic GMP but not cyclic AMP in platelets. LPS (200 μg/ml) significantly increased the production of nitrate within a 10-min incubation period. Furthermore, LPS also dose-dependently inhibited platelet aggregation induced by PDBu (30 nmol/1), a protein kinase C activator. These results indicate that the antiplatelet activity of E. coli LPS may be involved in the activation of a nitric oxide/cyclic GMP pathway in platelets, resulting in inhibition of platelet aggregation. Therefore, LPS-mediated alteration of platelet function may contribute to bleeding diathesis in septicemic and endotoxemic patients.

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