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June 21, 2013Arteriosclerosis Thrombosis and Vascular BiologyOpen Access

Thrombocytosis was detected in cGKI(L1/L1) and cGKI-SM mice due to elevated interleukin-6 levels, and antibody-mediated blockade of interleukin-6 normalized platelet counts in cGKI-SM mice.

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Population

Mouse models including conventional cGKI-null mutants (cGKI), gene-targeted cGKIα/β rescue mice, platelet…

Design

Preclinical

Authors

LZLin ZhangRŁRobert ŁukowskiFGFlorian Gaertner

Discussion

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Overview

IL-6 blockade normalizes platelets in cGKI-deficient mice; leaves open relevance to human thrombosis risk and requires clinical validation.

Structured PICO

P
Population
Mouse models including conventional cGKI-null mutants (cGKI(L1/L1)), gene-targeted cGKIα/β rescue mice (cGKI-SM), platelet factor 4-Cre(tg/+); cGKI(L2/L2) mice, and cGKI-deficient bone marrow-chimeras
I
Intervention
Antibody-mediated blockade of interleukin-6
O
Outcome
Platelet counts and megakaryopoiesissurrogate

Dysfunction of cGMP/cGKI signaling in nonhematopoietic cells leads to elevated interleukin-6 production and subsequent thrombocytosis, revealing a mechanism potentially associated with thrombosis.

Cite This Study

Zhang et al. (2013) studied this question.

synapsesocial.com/papers/6a7f2b217caf4fb4be694876https://doi.org/10.1161/atvbaha.113.301507
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  4. 4Multiple in vivo effects of interleukin-3 and interleukin-6 on murine megakaryocytopoiesis1991 · 73 citations
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