Apelin Promote Monocytes Adhesion To HUVECs Via 14-3-3 In PI3K Signaling Transduction Pathway

AIM: To observe the effects of apelin-13 induced monocytes (MCs) adhesion to human umbilical vein endothelial cells (HUVECs) via 14-3-3 in PI3K signaling transduction pathway. Further, investigated the new physiological function and signaling transduction pathway of apelin-APJ.Methods: Culturing HUVECs and MCs, MPO was used to identify effects of monocytes adhesion to HUVECs, Western Blotting was used to detecte the expression of VCAM-1, 14-3-3, p-PI3K and PI3K.Results: Apelin-13 induced adhesion of MCs to HUVECs in concentration dependence and time dependence, which reached their peaks at 1μmol/L and 12h, respectively. Similarly, apelin-13 induced the expression of HUVECs adhesion molecule VCAM-1 in concentration dependence and time dependence, which reached their peaks at 1μmol/L and 12h, respectively. The potent 14-3-3 inhibitor Difopein, PI3K inhibitor LY294002 inhibited the effect of apelin-13 induced MCs to HUVECs, while NOS inhibitor LNNA promoted the effect of apelin-13 induced MCs to HUVECs. Apelin-13 concentration–dependently induced PI3K phosphorylation and the expression of 14-3-3, which reached their peaks at 1μmol/L. Meanwhile, apelin-13 time– dependently induced PI3K phosphorylation and the expression of 14-3-3, which reached their peaks at 30min, 5min, respectively. Furthermore, the 14-3-3 inhibitor Difopein, PI3K inhibitor LY294002 significantly reduced PI3K phosphorylation and the expression of 14-3-3 and VCAM-1 in apelin-13 stimulated HUVECs. However, PI3K won,t influenced by apelin-13, LY294002 or Difopein in our study, at least. Conclusion: Apelin-13 promoted MCs adhesion to HUVECs via 14-3-3 in PI3K signaling transduction pathway.