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Diab Vasc Dis Res. 2014 Mar;11(2):121-4. doi: 10.1177/1479164113513912. Epub 2014 Jan 6.

Resistin increases platelet P-selectin levels via p38 MAPK signal pathway.

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1
Department of ICU, The First Affiliated Hospital of Shantou University Medical College, Shantou, PR China.

Abstract

Resistin, an adipokine associated with the metabolic syndrome, is believed to have a role in thrombotic conditions. This work analyses the effects of resistin on P-selectin expression using a combination of ex vivo human studies, in vivo animal models and in vitro cell cultures. Human platelets and vascular endothelial cells were incubated with resistin, with or without anti-Toll-like receptor 4 (TLR-4) or mitogen-activated protein kinases (MAPK) pathway inhibitors, whereas mice were treated with resistin infusion followed by analysis of P-selectin expression. Resistin increased both human and murine platelet P-selectin expression compared with controls (human: 48.02% ± 7.6% vs 35.12% ± 2.62%, p < 0.05; mouse: 8.17% ± 0.37% vs 4.44% ± 0.37%, p < 0.05), through the p38 MAPK pathway. In contrast, resistin had no effect on endothelial P-selectin production. We conclude that resistin induces platelet activation by increasing P-selectin expression through the p38 MAPK-dependent pathway. These data provide one mechanism for the prothrombotic state in individuals with the metabolic syndrome.

KEYWORDS:

P-selectin; Resistin; p38 MAPK; platelet

PMID:
24396117
DOI:
10.1177/1479164113513912
[Indexed for MEDLINE]
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