Abstract
Bone marrow stromal cells (BMSCs) can differentiate into vascular endothelial cells (VECs). It is regarded as an important solution to cure many diseases, such as ischemic diseases and diabetes. However, the mechanisms underlying BMSC differentiation into VECs are not well understood. Recent reports showed that CD163 expression was associated with angiogenesis. In this study, overexpression of CD163 in BMSCs elevated the protein level of the endothelial-associated markers CD31, Flk-1, eNOS, and VE-cadherin, significantly increased the proportion of Alexa Fluor 488-acetylated-LDL-positive VECs, and promoted angiogenesis on Matrigel. Furthermore, we demonstrated that CD163 acted downstream homeobox containing 1 (Hmbox1) and upstream fibroblast growth factor 2 (FGF-2). These data suggested that CD163 was involved in Hmbox1/CD163/FGF-2 signal pathway in BMSC differentiation into vascular endothelial-like cells. We found a new signal pathway and a novel target for further investigating the gene control of BMSC differentiation into a VEC lineage.
Highlights
Bone marrow stromal cells (BMSCs), due to their low immunogenicity and multilineage differentiation potential, promise as a main actor of cell-based therapeutic strategies [1]
Since many studies suggested the relationship between CD163 and endothelial differentiation, we intend to investigate the role of CD163 in the differentiation of BMSCs to vascular endothelial cells (VECs)
The results showed that protein levels of the endothelial-associated markers CD31 and Flk1 were undetectable in BMSCs transfected with pCMV6 empty vector, but they were observed in BMSCs transfected with pCMV6-CD163 at 0.8, 1.6 μg/mL (Figures 1(c) and 1(d))
Summary
Bone marrow stromal cells (BMSCs), due to their low immunogenicity and multilineage differentiation potential, promise as a main actor of cell-based therapeutic strategies [1] They are able to differentiate into various kinds of cells, including vascular endothelial cells (VECs), osteocytes, chondrocytes, adipocytes, and neural cells [2,3,4]. (3) Our previous study showed that chemical small molecule, 6-amino-2,3-dihydro-3-hydroxymethyl-1,4benzoxazine (ABO), could promote BMSC/mouse embryonic stem cell (mESC) differentiation into VECs by elevating homeobox containing 1 (Hmbox1) expression [2, 10]. We demonstrated that CD163 was positively regulated by Hmbox, and it could promote BMSC differentiation into vascular endothelial-like cells through enhancing FGF-2 signaling. The medium is replaced by basal DMEM with FGF2 (10 ng/mL) and rVEGF (10 ng/mL) incubated at 37∘C for another 24 h
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