Bone engineering in dog mandible: Coculturing mesenchymal stem cells with endothelial progenitor cells in a composite scaffold containing vascular endothelial growth factor

2016 ◽  
Vol 105 (7) ◽  
pp. 1767-1777 ◽  
Author(s):  
Arash Khojasteh ◽  
Farahnaz Fahimipour ◽  
Mohammad Jafarian ◽  
Davoud Sharifi ◽  
Shahrbanoo Jahangir ◽  
...  
Keyword(s):  
Stem Cells ◽  
Vascular Endothelial Growth Factor ◽  
Mesenchymal Stem Cells ◽  
Growth Factor ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Composite Scaffold ◽  
Vascular Endothelial ◽  
Endothelial Progenitor ◽  
Endothelial Growth Factor

scholarly journals Relationship between endothelial progenitor cells and vascular endothelial growth factor and its variation with exercise

2016 ◽  
Vol 137 ◽  
pp. 92-96 ◽  
Author(s):  
Juan A. Gagliardi ◽  
Neiva Maciel ◽  
José L. Castellano ◽  
Osvaldo Masoli ◽  
Verónica Miksztowicz ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Vascular Endothelial ◽  
Endothelial Progenitor ◽  
Endothelial Growth Factor

scholarly journals Vascular endothelial growth factor-A signaling in bone marrow-derived endothelial progenitor cells exposed to hypoxic stress

2013 ◽  
Vol 45 (21) ◽  
pp. 1021-1034 ◽  
Author(s):  
Brian R. Hoffmann ◽  
Jordan R. Wagner ◽  
Anthony R. Prisco ◽  
Agnieszka Janiak ◽  
Andrew S. Greene
Keyword(s):  
Bone Marrow ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Signaling Pathways ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Tube Formation ◽  
Vascular Endothelial ◽  
Endothelial Progenitor ◽  
Endothelial Growth Factor

Bone marrow-derived endothelial progenitor cells (BM-EPCs) are stimulated by vascular endothelial growth factor-A (VEGF-A) and other potent proangiogenic factors. During angiogenesis, an increase in VEGF-A expression stimulates BM-EPCs to enhance endothelial tube formation and contribute to an increase in microvessel density. Hypoxia is known to produce an enhanced angiogenic response and heightened levels of VEGF-A have been seen in oxygen deprived epithelial and endothelial cells, yet the pathways for VEGF-A signaling in BM-EPCs have not been described. This study explores the influence of hypoxia on VEGF-A signaling in rat BM-EPCs utilizing a novel proteomic strategy to directly identify interacting downstream components of the combined VEGF receptor(s) signaling pathways, gene expression analysis, and functional phenotyping. VEGF-A signaling network analysis following liquid chromatographic separation and tandem mass spectrometry revealed proteins related to inositol/calcium signaling, nitric oxide signaling, cell survival, cell migration, and inflammatory responses. Alterations in BM-EPC expression of common angiogenic genes and tube formation in response to VEGF-A during hypoxia were measured and combined with the proteomic analysis to enhance and support the signaling pathways detected. BM-EPC tube formation assays in response to VEGF-A exhibited little tube formation; however, a cell projection/migratory phenotype supported the signaling data. Additionally, a novel assay measuring BM-EPC incorporation into preformed endothelial cell tubes indicated a significant increase of incorporated BM-EPCs after pretreatment with VEGF-A during hypoxia. This study verifies known VEGF-A pathway components and reveals several unidentified mechanisms of VEGF-A signaling in BM-EPCs during hypoxia that may be important for migration to sites of vascular regeneration.

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