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Velazquez OCAngiogenesis and vasculogenesis: inducing the growth of new blood vessels and wound healing by stimulation of bone marrow-derived progenitor cell mobilization and homing. J Vasc Surg 45(Suppl A):A39-A47

Department of Surgery, University of Pennsylvania Medical Center, Philadelphia, PA 19104-4283, USA.
Journal of Vascular Surgery (Impact Factor: 2.98). 07/2007; 45 Suppl A(6):A39-47. DOI: 10.1016/j.jvs.2007.02.068
Source: PubMed

ABSTRACT During embryonic development, the vasculature is among the first organs to form and is in charge of maintaining metabolic homeostasis by supplying oxygen and nutrients and removing waste products. As one would expect, blood vessels are critical not only for organ growth in the embryo but also for repair of wounded tissue in the adult. An imbalance in angiogenesis (a time-honored term that globally refers to the growth of new blood vessels) contributes to the pathogenesis of numerous malignant, inflammatory, ischemic, infectious, immune, and wound-healing disorders. This review focuses on the central role of the growth of new blood vessels in ischemic and diabetic wound healing and defines the most current nomenclature that describes the neovascularization process in wounds. There are now two well-defined, distinct, yet interrelated processes for the formation of postnatal new blood vessels, angiogenesis, and vasculogenesis. Reviewed are recent new data on vasculogenesis that promise to advance the field of wound healing.

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    • "The presence of the initial hernia and the high risk of recurrence are indicative of a breakdown in the normal wound healing process. One central component of the wound healing process is the restoration of the metabolic capacity of damaged tissue through angiogenesis and vasculogenesis, two separate but related processes [2]. "
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    ABSTRACT: Introduction. In adipose tissue healing, angiogenesis is stimulated by adipose-derived stromal stem cells (ASCs). Ventral hernia repair (VHR) patients are at high risk for wound infections. We hypothesize that ASCs from VHR patients are less vasculogenic than ASCs from healthy controls. Methods. ASCs were harvested from the subcutaneous fat of patients undergoing VHR by the component separation technique and from matched abdominoplasty patients. RNA and protein were harvested on culture days 0 and 3. Both groups of ASCs were subjected to hypoxic conditions for 12 and 24 hours. RNA was analyzed using qRT-PCR, and protein was used for western blotting. ASCs were also grown in Matrigel under hypoxic conditions and assayed for tubule formation after 24 hours. Results. Hernia patient ASCs demonstrated decreased levels of VEGF-A protein and vasculogenic RNA at 3 days of growth in differentiation media. There were also decreases in VEGF-A protein and vasculogenic RNA after growth in hypoxic conditions compared to control ASCs. After 24 hours in hypoxia, VHR ASCs formed fewer tubules in Matrigel than in control patient ASCs. Conclusion. ASCs derived from VHR patients appear to express fewer vasculogenic markers and form fewer tubules in Matrigel than ASCs from abdominoplasty patients, suggesting decreased vasculogenic activity.
    03/2014; 2014(6):983715. DOI:10.1155/2014/983715
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    • "Both cell types are indispensible for vascular development which depends upon the processes of angiogenesis and vasculogenesis. While angiogenesis describes the formation of neovessels through the proliferation and migration of ECs from a mature vascular network, vasculogenesis is a process involving the differentiation and incorporation of EPCs in de novo-formed vessels [Velazquez, 2007]. The increased proliferation of both ECs and EPCs in contact with the modified matrices studied here indicates that these matrices provide a conducive environment for both vascularization processes to take place. "
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    ABSTRACT: The use of implantable biomaterials, such as artificial skin substitutes used for dermal defects, remains limited by the low angiogenic potential of these products. The rapid in vivo degradation of growth factors contributes to the limiting of angiogenesis in biomaterials. Here, we report on collagen sponges in which vascular endothelial growth factor (VEGF) was immobilized through physical binding to heparin, covalently incorporated in the matrix via cross-linking with 1-ethyl-3-(3-dimethylaminopropyl)carbodiimide (EDC) and N-hydroxysuccinimide. The in vitro release of VEGF over time and endothelial cell proliferation were investigated in matrices modified at varying heparin to EDC ratios either nonloaded or loaded with VEGF. ELISA demonstrated a significantly slower in vitro release of VEGF over a period of 5 days from heparinized matrices as compared to their unmodified and cross-linked counterparts. The effects of these modifications on the proliferation of endothelial cells and endothelial progenitor cells were evaluated after 1, 3 and 5 days either according to the bromodeoxyuridine assay or total cell counting with a Neubauer chamber. The endothelial and endothelial progenitor cells cultured in contact with heparinized matrices loaded with VEGF revealed both the highest rate of DNA synthesis and the highest total cell count. Furthermore, these results show that the cross-linking of collagen matrices - both in the presence and absence of heparin - leads to increases of the proliferative activities. We can assume that these changes lead to matrices with increased angiogenic capabilities.
    Cells Tissues Organs 08/2009; 191(2):96-104. DOI:10.1159/000231473 · 2.14 Impact Factor
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