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Mol Cell Biochem. 2013 May;377(1-2):229-36. doi: 10.1007/s11010-013-1592-z. Epub 2013 Feb 23.

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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  • 1Key Laboratory of Atherosclerosis in Universities of Shandong, Institute of Atherosclerosis, Taishan Medical University, Taian, Shandong, People's Republic of China.

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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