Id-1 mediated E2-2 to regulate PI3K/Akt signaling pathway and influenced endothelial progenitor cell increase
Abstract：Objective To explore the associations between Id-1,E2-2 and PI3K/Akt pathway for increase of EPCs. MethodsIn the EPCs cell model,we used immune coprecipitation test to detect the association between Id-1 and E2-2.We overexpressed orinterfered Id -1 or E2 -2,and used CCK 8 method to detect cell increase;RT -PCR and Western blotting technique to detectexpression of PI3K,and Akt levels. Results Immune coprecipitation test found that there was protein-protein interaction betweenId-1 and E2-2. Compared with the control group,overexpression of Id -1 could decrease the E2-2 expression level,and increase theexpression of PI3K/Akt,which lead to inhanced cell proliferation ability. Overexpressing E2-2 reduced the expression of PI3K/Aktand cell proliferation. Co-transfection Id-1 and E2-2 showed that both proteins could influence the expression of PI3K/Akt levelsynergetically. Conclusion There was protein-protein interaction between Id-1 and E2-2;Id-1 has positive regulatory role for PI3K/Akt while E2-2 has a negative regulatory role. The Id-1 and E2-2 could coordinate to control the PI3K/Akt signal pathway,thusaffecting the increase of the EPCs.
Keywords：Id1E2-2increaseEPCsPI3k/Akt pathway
Publication Date：2017-01-01
Online Publishing Date：2025-08-15(First online date of this platform, not the publication date of the document)
Pages：5( 5-9 )