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Apolipoprotein A-I mimetic peptide reverse D-4F improves the biological functions of mouse bone marrow-derived late EPCs via PI3K/AKT/eNOS pathway

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Abstract

Apolipoprotein A-I (ApoA-I) mimetic peptide inhibits the development of atherosclerosis (AS) in apolipoprotein E-deficient mice; however, the underlying mechanism remains unclear. Endothelial progenitor cells (EPCs) can prevent AS progression through repairing proatherogenic factors impaired endothelium. In the present study, we examined the effect of reverse D-4F, one of apoA-I mimetic peptide on the proliferation, migration, and tube formation of mouse bone marrow-derived late EPCs. The present study showed that reverse D-4F (10–100 μg/ml) significantly improved the proliferation, migration, and tube formation of EPCs in a dose-dependent manner, and activated phospho-AKT at serine residue 473 and phospho-eNOS at serine residue 1177. LY294002 (PI3-kinase inhibitor) and L-NAME (NOS inhibitor) significantly inhibited reverse D-4F mediated improvement of EPCs biological functions, and LY294002 significantly decreased reverse D-4F stimulated activation of phospho-AKT (473) and phospho-eNOS (1177). The results indicate that reverse D-4F mediated improvement of EPCs functions is dependent on the PI3K/AKT/eNOS pathway.

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Acknowledgments

This study was supported by the National Natural Science Foundation of China (No. 30971098), the Province Natural Science Foundation of Shandong (No.Z2008C03), the Province Natural Science Foundation of Shandong (No.ZR2012HL18), Taishan Scholars Project Funding from Shandong Province, Natural Science Foundation of Taishan Medical University (2011ZR004), and Province Chinese Medicine Science and Technology Development Project of Shandong (2011-228).

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Correspondence to Shucun Qin.

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Nana Yang and Shutong Yao equally contributed to this study.

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Yang, N., Yao, S., Wang, M. et al. Apolipoprotein A-I mimetic peptide reverse D-4F improves the biological functions of mouse bone marrow-derived late EPCs via PI3K/AKT/eNOS pathway. Mol Cell Biochem 377, 229–236 (2013). https://doi.org/10.1007/s11010-013-1592-z

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