BMP9 Induces Cord Blood-Derived Endothelial Progenitor Cell Differentiation and Ischemic Neovascularization via ALK1.

Title
BMP9 Induces Cord Blood-Derived Endothelial Progenitor Cell Differentiation and Ischemic Neovascularization via ALK1.
Authors
이욱빈Jihye KimMinhyung KimYoonjeong JeongHyojin ParkJa-Young KwonYoung-Myeong KimDaehee HwangYoung-Guen Kwon
Issue Date
2015-09
Publisher
Arteriosclerosis, thrombosis, and vascular biology
Citation
VOL 35, NO 9-2031
Abstract
Objective Modulating endothelial progenitor cells (EPCs) is essential for therapeutic angiogenesis, and thus various clinical trials involving EPCs are ongoing. However, the identification of environmental conditions and development of optimal methods are required to accelerate EPC-driven vasculogenesis. Approach and Results We evaluated gene expression profiles of cord blood-derived EPCs and endothelial cells to identify the key factors in EPCendothelial cell differentiation and to show that transforming growth factor- family members contribute to EPC differentiation. The expression levels of activin receptor-like kinase 1 (ALK1) and its high-affinity ligand, bone morphogenetic protein 9 (BMP9) were markedly changed in EPCendothelial cell differentiation. Interestingly, BMP9 induced EPCendothelial cell differentiation and EPC incorporation into vessel-like structures by acting on ALK1 expressed on EPCs in vitro. BMP9 also induced neovascularization in mice with hindlimb ischemia by increasing vessel formation and the incorporation of EPCs into vessels. Conversely, neovascularization was impaired when ALK1 signaling was blocked. Furthermore, EPCs exposed to either short- or long-term BMP9 stimulation demonstrated these functions in EPC-mediated neovascularization. Conclusions Collectively, our results indicated that BMP9/ALK1 augmented vasculogenesis and angiogenesis, and thereby enhanced neovascularization. Thus, we suggest that BMP9/ALK1 may improve the efficacy of EPC-based therapies for treating ischemic diseases.
URI
http://pubs.kist.re.kr/handle/201004/69297
ISSN
1079-5642
Appears in Collections:
KIST Publication > Article
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