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April 14, 2006Journal of Biological ChemistryOpen Access

A Phosphoinositide 3-Kinase-AKT-Nitric Oxide-cGMP Signaling Pathway in Stimulating Platelet Secretion and Aggregation

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Population

Platelets, including Akt-1 knock-out platelets

Comparison

Akt inhibitors, PI3K inhibitors, 8-bromo-cGMP… vs Untreated or wild-type platelets

Design

Preclinical

Authors

ASAleksandra StojanovićJMJasna MarjanovicVBViktor Brovkovych

Discussion

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Overview

Extends the platelet signaling map via Akt-NO-cGMP; leaves open whether pathway inhibition alters thrombosis in vivo.

Structured PICO

P
Population
Platelets, including Akt-1 knock-out platelets
I
Intervention
Akt inhibitors, PI3K inhibitors, 8-bromo-cGMP, or sodium nitroprusside
C
Comparator
Untreated or wild-type platelets
O
Outcome
Platelet NO synthesis, cGMP elevation, platelet secretion, and aggregationsurrogate

This study delineates a novel platelet activation pathway involving sequential activation of PI3K, Akt, nitric-oxide synthase 3, sGC, and cGMP-dependent protein kinase.

Cite This Study

Stojanović et al. (2006) studied this question.

synapsesocial.com/papers/6a70c40ff44fa9f079de75f4https://doi.org/10.1074/jbc.m512378200
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