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

作者：Yang, Nana; Yao, Shutong; Wang, Mengzan; Jiao, Peng; Zhang, Ying; Qin, Shucun^*

来源：Molecular and Cellular Biochemistry, 2013, 377(1-2): 229-236.

DOI：10.1007/s11010-013-1592-z

• Apolipoprotein A-I mimetic peptide
• Endothelial progenitor cells
• eNOS

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 mu g/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.

• 出版日期2013-5
• 单位山东大学; 聊城市人民医院; 山东第一医科大学