November 1, 1984Journal of Biological ChemistryOpen Access

Thrombin-induced release of von Willebrand factor from endothelial cells is mediated by phospholipid methylation. Prostacyclin synthesis is independent of phospholipid methylation.

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Population

Cultured human umbilical vein endothelial cells

Design

Preclinical

Authors

PGPhilip G. de GrootSynapse (Netherlands)MGMervin D. GonsalvesDutch Blood Transfusion Society CLC. Loesberg

Discussion

Member takes

Implication

Distinguishes separable thrombin pathways in endothelium; hypothesis-generating for selective modulation in vascular models.

Structured PICO

Population

Cultured human umbilical vein endothelial cells

Intervention

Thrombin treatment (with or without inhibitors/stimulators like 3-deazaadenosine, PMA, A23187, EDTA)

Outcome

Release of von Willebrand factor and prostacyclin synthesis, along with phospholipid methylation and Ca2+ influxsurrogate

This study demonstrates that thrombin triggers distinct metabolic pathways in endothelial cells for von Willebrand factor release (dependent on phospholipid methylation and Ca2+) and prostacyclin synthesis (independent of these factors).

Cite This Study

Groot et al. (1984) studied this question.

synapsesocial.com/papers/6a90e578263aa8e25c73cb5b https://doi.org/10.1016/s0021-9258(18)90698-8

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Thrombin-induced release of von Willebrand factor from endothelial cells is mediated by phospholipid methylation. Prostacyclin synthesis is independent of phospholipid methylation.

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Thrombin-induced release of von Willebrand factor from endothelial cells is mediated by phospholipid methylation. Prostacyclin synthesis is independent of phospholipid methylation.

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider