Journal
EUROPEAN CELLS & MATERIALS
Volume 21, Issue -, Pages 459-469Publisher
AO RESEARCH INSTITUTE DAVOS-ARI
DOI: 10.22203/eCM.v021a34
Keywords
Endothelial progenitor cells; Ginkgolide B; proliferation; angiogenesis; Akt; endothelial nitric oxide synthase ( eNOS); p38
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Funding
- Key Program of National Natural Science Foundation of China-Guangdong Joint Funding [u0732001]
- Key International S&T Cooperation Project of Ministry of Science and Technology of the People's Republic of China [2005DFA30570]
- International S&T Cooperation Network Project of Danish Council for Strategic Research for Individualized Musculoskeletal Regeneration and Reconstruction Network [2101-07-0120]
- Project of Chinese-German Junior Research Group on Biotechnology [2009004]
- Guangdong Natural Science Foundation [8151008901000167]
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Bone marrow-derived, circulating endothelial progenitor cells (EPCs) contribute to neovascularization in various diseases, and represent a very interesting alternative cell source for enhancing vasculogenesis in regenerative medicine. In this study, we investigated the effects of Ginkgolide B (GB) on proliferation and differentiation of EPCs, and the involved signaling pathway in vitro. EPC proliferation, migration, adhesion and angiogenesis activities were assessed with the WST-8 assay, Transwell chamber assay, cell counting and angiogenesis kit, respectively. Apoptosis was detected with annexin V and propidium iodide staining. The protein expression of angiogenesis-related makers was detected by Western blot, and related gene expression was determined by real-time polymerase chain reaction (RT-PCR). The results showed that GB promoted the proliferation and endothelial gene expression, and markedly enhanced vascular endothelial growth factor-induced migration response and the capability to incorporate into the vascular networks in EPCs. GB protected EPCs from H2O2-induced cell death. GB induced the phosphorylation of eNOS, Akt and p38, which in turn promoted cell proliferation and function. In conclusion, the present study demonstrates that GB, at a near medical applied dose, increases the number and functional activities of EPCs with involvement of Akt/endothelial nitric oxide synthase and mitogen-activated protein kinase (MAPK)/p38 signal pathways. These findings raise the intriguing possibility that GB may play an important role in the protection and revascularization of blood vessels.
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