To measure blood vessel density after cell transplantation, anti-CD31 IHC staining of liver sections was performed. As shown in Fig. 7A, more CD31 positive blood vessels were observed in the HD group than those in the RD and PBS groups. Further qRT-PCR Venlafaxine analysis of Liproxstatin-1 pro-angiogenic gene expression was consistent with the above observation, that a higher level of VEGF-A and angiopoietin-1 expression were observed in livers transplanted with HD cultured cells, accompanied with an increased expression of VEGF receptor-2 but decreased expression of Tie-2. Recent advances in stem cell research have revealed that bone marrow-derived cells, including HSCs, MSCs, EPCs, and BMNCs, could significantly protect liver function after injury. In the present study, we demonstrated that an EPC enriched population from a novel HD culture of bone marrow cells, displayed better antifibrogenic potential in the treatment of chronic liver injury. The antifibrogenic effect was determined by biochemical and histological evidence. Previously, we demonstrated that EPCs could be expanded in HD culture without pre-coating culture dishes and addition of extra growth factors, which is a simple and cost-effective method for in vitro expansion of bone marrow EPCs. On the contrary, the RD culture, which has been adopted widely for MSCs culture, could efficiently expand MSCs with loss of EPCs during cell passage. Although no previous reports have compared the efficacy of EPCs to MSCs in the treatment of chronic liver injury, the current work provides evidence that bone marrow cells enriched for EPCs could function better than relatively pure MSCs in vivo. The mechanism of action can be explained as follows: first, more cells from the HD culture homed to and survived in the injured liver after injection ; second, a lower level of the pro-fibrogenic factors, TGF-b and PDGF-B, were expressed in the liver of the HD group; third, matrix degradation enzyme MMP-2 were highly expression in HD group; fourth, cell proliferation was stimulated through higher expression of HGF in the HD group; and finally, more blood vessels were formed, induced by higher expressions of VEGF-A and Ang-1 in the HD group.