Journal
DIABETES & VASCULAR DISEASE RESEARCH
Volume 11, Issue 2, Pages 121-124Publisher
SAGE PUBLICATIONS LTD
DOI: 10.1177/1479164113513912
Keywords
platelet; p38 MAPK; P-selectin; Resistin
Funding
- Guangdong Provincial Science & Technology Foundation [2009B030801325]
- Medical Scientific Research Foundation of Guangdong Province [B2011218]
- National Natural Science Foundation of China [81070413]
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available