Role and mechanism of ABI3BP in angiotensin Ⅱ-induced endothelial progenitor cell dysfunction

Ren Mingxia; Xie Huaqiang; Tu Qiang; Cao Zheng

doi:10.3969/j.issn.1009-0126.2024.08.020

Abstract：Objective To investigate the role and mechanism of ABI family member 3-binding pro-tein(ABI3BP)in dysfunction of endothelial progenitor cells(EPC)induced by angiotensin Ⅱ(Ang Ⅱ).Methods EPC were divided into sh-RNA negative control(sh-NC)group(transfected with LV-scramble-shRNA+PBS),sh-ABI3BP group(transfected with LV-ABI3BP-shRNA+PBS),sh-NC+Ang Ⅱ group(transfected with LV-scramble-shRNA+Ang Ⅱ)and sh-ABI3BP+Ang Ⅱ group(transfected with LV-ABI3BP-shRNA+Ang Ⅱ)to investigate the effect of silencing ABI3BP on the dysfunction of EPC induced by Ang Ⅱ.Transwell assay,adhesion assay,Matrigel tube formation assay,and TUNEL staining were performed respectively to detect the migration,adhesion and tube formation abilities and cell apoptosis in above cell groups.The expression chan-ges in integrin-β1/FAK/P53 signaling pathway were detected by Western blotting.Results Com-pared to the sh-NC group,the sh-NC+AngⅡ group showed significant decreases in the numbers of migratory cells,adhesion cells,and tubule formation,along with increases in the apoptotic rate and the expression levels of Integrin β1,p-FAK,and P53(P＜0.05).While,the sh-ABI3BP+AngⅡ group had obviously more migratory cells(88.67±8.33 vs 62.33±7.37 units,P＜0.05),adhe-sion cells(104.33±6.03 vs 68.33±10.05 units,P＜0.05),and tubule formation(36.33±3.21 vs 19.33±3.06 units,P＜0.05),while decreased apoptotic rate and expression levels of integrin-β1,p-FAK and P53 protein when compared with the sh-NC+AngⅡ group(P＜0.05).Conclusion Ang Ⅱ can up-regulate the expression of ABI3BP,and knockdown of ABI3BP can improve Ang Ⅱ-induced EPC dysfunction,which may be related to its inhibition on integrin-β1/FAK/P53 signa-ling pathway.