AMD3100 Mobilizes Endothelial Progenitor Cells in Mice, But Inhibits Its Biological Functions by Blocking an Autocrine/Paracrine Regulatory Loop of Stromal Cell Derived Factor-1 In Vitro

2007 ◽  
Vol 50 (1) ◽  
pp. 61-67 ◽  
Author(s):  
Yangguang Yin ◽  
Lan Huang ◽  
Xiaohui Zhao ◽  
Yuqiang Fang ◽  
Shiyong Yu ◽  
...  
2016 ◽  
Vol 2016 ◽  
pp. 1-18 ◽  
Author(s):  
Shih-Ya Tseng ◽  
Ting-Hsing Chao ◽  
Yi-Heng Li ◽  
Chung-Lung Cho

This study investigated the effect of cilostazol on proangiogenesis functions in human early endothelial progenitor cells (EPCs)in vitroand the therapeutic implication of hybrid therapy with cilostazol and human early EPCsin vivo. Cilostazol significantly increased colony-forming units and enhanced differentiation of EPCs toward endothelial lineage. Treatments resulted in antiapoptotic effects and stimulated proliferation and migration andin vitrovascular tube formation through activation of stromal cell-derived factor-1 (SDF-1)/C-X-C chemokine receptor type 4 (CXCR4)/phosphatidylinositol-3 kinase (PI3K)/Akt signaling pathway. Blood flow recovery and capillary density in murine ischemic hindlimbs were significantly improved in cilostazol-treated, human early EPCs-treated, and cotreatment groups. The effects were attenuated with SDF-1αinhibition. Plasma SDF-1αlevels were significantly higher in 3 active treatment groups after surgery, with greatest effects observed in hybrid therapy. The angiogenic effects of transplanted EPCs pretreated with cilostazolex vivowere superior to untreated EPCs usingin vivoMatrigel assay. Implanted EPCs were incorporated into the capillary, with pretreatment or cotreatment with cilostazol resulting in enhanced effects. Taken together, cilostazol promotes a large number of proangiogenic functions in human early EPCs through activation of SDF-1/CXCR4/PI3K/Akt signaling, and hybrid therapy provides a synergistic effectin vivo. Cotreatment may be beneficial in ischemic disease.


2015 ◽  
Vol 135 (2) ◽  
pp. 340e-350e ◽  
Author(s):  
Edwin Chang ◽  
Josemaria Paterno ◽  
Dominik Duscher ◽  
Zeshaan N. Maan ◽  
Jerry S. Chen ◽  
...  

Circulation ◽  
2008 ◽  
Vol 117 (2) ◽  
pp. 206-215 ◽  
Author(s):  
Konstantinos Stellos ◽  
Harald Langer ◽  
Karin Daub ◽  
Tanja Schoenberger ◽  
Alexandra Gauss ◽  
...  

2017 ◽  
Vol 10 ◽  
pp. 117955141774398 ◽  
Author(s):  
Roberto Negro ◽  
Eupremio Luigi Greco ◽  
Giacomo Greco

Background: It is postulated that the ability of dipeptidyl peptidase-4 inhibitors (DPP-4-i) to increase circulating endothelial progenitor cells (EPCs) may be at least partly mediated by active stromal cell–derived factor 1α (SDF-1α) (a pivotal mediator of stem cell mobilization from the bone marrow). As other DPP-4-i were demonstrated to increase EPC concentrations, in this study, we sought to investigate the ability of the DPP-4-i alogliptin in modifying EPCs and SDF-1α, in patients with good and poor diabetes control. Methods: Two groups of diabetic patients on metformin were divided by hemoglobin A1c (HbA1c): Group A—those with HbA1c ≤6.5% (28 patients) and Group B—those with HbA1c 7.5% to 8.5% (31 patients). Both groups received alogliptin 25 mg/daily for 4 months. At baseline and 4 months later, clinical, laboratory parameters, EPCs, and active SDF-1α were determined. Results: After 4-month treatment with alogliptin, either Group A or Group B showed reduced HbA1c levels and concomitant similar increase in EPCs and active SDF-1α. Conclusions: Alogliptin showed significant benefits in increasing EPCs and active SDF-1α either in good or poor diabetes control. The study demonstrated that similar to other DPP-4-i, also alogliptin is able to increase EPC concentrations, suggesting the existence of a class effect mediated by SDF-1α. The extent of increase in EPCs is independent from baseline diabetes control.


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