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Insulin-like growth factor 1 opposes the effects of C-reactive protein on endothelial cell activation

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Abstract

Emerging evidence demonstrates that high plasma C-reactive protein (CRP) levels or low plasma insulin-like growth factor 1 (IGF-1) concentrations may be separately associated with the increased risk of coronary artery disease or myocardial infarction. Interestingly, animal model studies and epidemiological investigations indicate that circulating IGF-1 and CRP levels have an inverse correlation. The present study aims to evaluate if IGF-1 can directly oppose the effects of CRP on endothelial cell (EC) activation. We found that IGF-1 rescues endothelial nitric oxide synthase activity and decreases the release of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 from ECs. We also showed that IGF-1 antagonizes the effects of CRP by activating the PI3K/Akt pathway and suppressing the JNK/c-Jun and MAPK p38/ATF2 signaling pathways, rather than inhibiting ERK1/2 activity. These findings provide evidence of the physiopathological mechanisms of endothelial activation and novel insights into the protective properties of IGF-1.

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Acknowledgments

This study was supported by the National Natural Science Foundation of China (No. 81300151), Research Fund for the Doctoral Program of Higher Education of China (No. 20124423120001), Research Project for Post-doctoral Program of Guangzhou city (No.310109-002), Research Fund for the Doctoral Program of Guangzhou Medical University (No.52010202), and Foundation for Distinguished Young Talents in Higher Education of Guangdong, China (No. 2012LYM_0111).

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Correspondence to Shi-Ming Liu.

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Liu, SJ., Zhong, Y., You, XY. et al. Insulin-like growth factor 1 opposes the effects of C-reactive protein on endothelial cell activation. Mol Cell Biochem 385, 199–205 (2014). https://doi.org/10.1007/s11010-013-1828-y

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  • DOI: https://doi.org/10.1007/s11010-013-1828-y

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