Cxcr7 Inhibits Fibrosis Via Wnt/Beta-Catenin Pathways During The Process Of Angiogenesis In Human Umbilical Vein Endothelial Cells

Although SDF-1/CXCR7 plays an important role in angiogenesis, the function and the pathway of the SDF-1/CXCR7 axis might depend on the cell type or tissue origin and not fully understood. In this study, we investigated the effect of CXCR7 in SDF-1-induced proliferation, migration, apoptosis, tube formation, and endothelial-to-mesenchymal transition (EndMT) of human umbilical vein endothelial cells (HUVECs), and the potential pathway of SDF-1/CXCR7. We confirmed that the silencing of CXCR7 inhibited the proliferation of HUVECs and contributed the apoptosis, while overexpressed CXCR7 increased SDF-1-induced HUVECs migration and tube formation. However, upregulated CXCR7 inhibited the expression of alpha-SMA, suggesting that CXCR7 might attenuate EndMT. In addition, overexpressed CXCR7 activated AKT and ERK signaling pathways but suppressed Wnt/beta-catenin pathways in HUVECs. The inhibition of Wnt/beta-catenin pathways decreased the expression of alpha-SMA. Altogether, these results suggest that CXCR7 might inhibit fibrosis via Wnt/beta-catenin pathways during the process of angiogenesis.