[Mechanisms of prostaglandin E2-induced bone marrow-derived progenitor cell differentiation]

To identify the functions and mechanisms of prostaglandin E2 (PGE2)-induced bone marrow-derived progenitor cells (BMPCs) maturation and its involved angiogenesis.

BMPCs harvested by flushing through the femoral and tibial bones and cultured. This population of cells was identified by immunofluorescence staining. From which, 1 μmol/L PGE2 was taken, and quantitative-PCR (Q-PCR) and Western blot were used to detect the expressions of endothelial markers and Kruppel like factor 2 (KLF2) in BMPCs. In vitro tube formation assay was performed to demonstrate the capacity of angiogenesis. Furthermore, PGE2 and its receptors EP2 and EP4 agonists were used to elucidate the regulation of PGE2 to KLF2.

C-kit, von Willebrand factor (vWF) and vascular endothelial cadherin expressed in BMPCs. Treatment with PGE2 (1 μmol/L) significantly increased the differentiation of BMPCs. The mRNA levels of endothelial markers platelet endothelial cell adhesion molecule-1 (PECAM-1/CD31) and endothelial nitric oxide synthase (eNOS), were significantly upregulated in about 2 folds by PGE2 detected with Q-PCR assay. Matrigel tube formation assay also demonstrated PGE2 enhanced the ability of angiogenesis in BMPCs. In addition, the expression of KLF2 increased in more than 2 folds with PGE2 treatment compared with the control. Such effect of PGE2 could be blocked by EP4 blocking peptide.

Promoting the differentiation of BMPCs, PGE2 reinforced their angiogenesis by binding to the receptor of EP4 in a KLF2-dependent manner.