The Experts below are selected from a list of 324 Experts worldwide ranked by ideXlab platform

Stephen D Charnockjones - One of the best experts on this subject based on the ideXlab platform.

  • wnt5a mediated non canonical wnt signalling regulates human Endothelial Cell Proliferation and migration
    Biochemical and Biophysical Research Communications, 2008
    Co-Authors: Chingwen Cheng, S K Smith, Stephen D Charnockjones
    Abstract:

    Cell to Cell interaction is one of the key processes effecting angiogenesis and Endothelial Cell function. Wnt signalling is mediated through Cell-Cell interaction and is involved in many developmental processes and Cellular functions. In this study, we investigated the possible function of Wnt5a and the non-canonical Wnt pathway in human Endothelial Cells. We found that Wnt5a-mediated non-canonical Wnt signalling regulated Endothelial Cell Proliferation. Blocking this pathway using antibody, siRNA or a down-stream inhibitor led to suppression of Endothelial Cell Proliferation, migration, and monolayer wound closure. We also found that the mRNA level of Wnt5a is up-regulated when Endothelial Cells are treated with a cocktail of inflammatory cytokines. Our findings suggest non-canonical Wnt signalling plays a role in regulating Endothelial Cell growth and possibly in angiogenesis.

G. Gagnon - One of the best experts on this subject based on the ideXlab platform.

  • effects of calcium and thrombin on growth factor release from platelet concentrates kinetics and regulation of Endothelial Cell Proliferation
    Biomaterials, 2004
    Co-Authors: I. Martineau, E Lacoste, G. Gagnon
    Abstract:

    Abstract Platelet concentrates (PCs) constitute new biological mediators used in osseous reconstructive surgery. In this study, we assessed (i) the effects of various concentrations of calcium and thrombin on the kinetics of platelet-derived growth factor (PDGF-BB), transforming growth factor-beta1(TGF-β1), basic fibroblast growth factor (bFGF), and vascular Endothelial growth factor (VEGF) release by PCs and (ii) the contribution of PC supernatants to Endothelial Cell Proliferation. Our results indicate that high concentrations of calcium (Ca) and thrombin (Thr) trigger an immediate and significant increase in bFGF, TGF-β1 and PDGF-BB concentrations. Thereafter, PDGF-BB, VEGF and TGF-β1 levels remained generally constant over a 6-day period while a decrease in bFGF concentrations was noted after 24 h. Lower Ca and Thr concentrations tended to reduce and delay growth factors release from PCs. Endothelial Cell Proliferation was greatly enhanced with PC supernatants (mean: 20-fold increase). This was especially evident when Endothelial Cells were treated with supernatants harvested early after PC treatment with high concentrations of Ca and Thr or later after PC treatment with low Ca and Thr concentrations. Additional research aiming to measure the effects of Ca and Thr on bone formation in vivo is needed.

  • Effects of calcium and thrombin on growth factor release from platelet concentrates: Kinetics and regulation of Endothelial Cell Proliferation
    Biomaterials, 2004
    Co-Authors: I. Martineau, E Lacoste, G. Gagnon
    Abstract:

    Platelet concentrates (PCs) constitute new biological mediators used in osseous reconstructive surgery. In this study, we assessed (i) the effects of various concentrations of calcium and thrombin on the kinetics of platelet-derived growth factor (PDGF-BB), transforming growth factor-beta1(TGF-β1), basic fibroblast growth factor (bFGF), and vascular Endothelial growth factor (VEGF) release by PCs and (ii) the contribution of PC supernatants to Endothelial Cell Proliferation. Our results indicate that high concentrations of calcium (Ca) and thrombin (Thr) trigger an immediate and significant increase in bFGF, TGF-β1 and PDGF-BB concentrations. Thereafter, PDGF-BB, VEGF and TGF-β1 levels remained generally constant over a 6-day period while a decrease in bFGF concentrations was noted after 24h. Lower Ca and Thr concentrations tended to reduce and delay growth factors release from PCs. Endothelial Cell Proliferation was greatly enhanced with PC supernatants (mean: 20-fold increase). This was especially evident when Endothelial Cells were treated with supernatants harvested early after PC treatment with high concentrations of Ca and Thr or later after PC treatment with low Ca and Thr concentrations. Additional research aiming to measure the effects of Ca and Thr on bone formation in vivo is needed. © 2003 Elsevier Ltd. All rights reserved.

I. Martineau - One of the best experts on this subject based on the ideXlab platform.

  • effects of calcium and thrombin on growth factor release from platelet concentrates kinetics and regulation of Endothelial Cell Proliferation
    Biomaterials, 2004
    Co-Authors: I. Martineau, E Lacoste, G. Gagnon
    Abstract:

    Abstract Platelet concentrates (PCs) constitute new biological mediators used in osseous reconstructive surgery. In this study, we assessed (i) the effects of various concentrations of calcium and thrombin on the kinetics of platelet-derived growth factor (PDGF-BB), transforming growth factor-beta1(TGF-β1), basic fibroblast growth factor (bFGF), and vascular Endothelial growth factor (VEGF) release by PCs and (ii) the contribution of PC supernatants to Endothelial Cell Proliferation. Our results indicate that high concentrations of calcium (Ca) and thrombin (Thr) trigger an immediate and significant increase in bFGF, TGF-β1 and PDGF-BB concentrations. Thereafter, PDGF-BB, VEGF and TGF-β1 levels remained generally constant over a 6-day period while a decrease in bFGF concentrations was noted after 24 h. Lower Ca and Thr concentrations tended to reduce and delay growth factors release from PCs. Endothelial Cell Proliferation was greatly enhanced with PC supernatants (mean: 20-fold increase). This was especially evident when Endothelial Cells were treated with supernatants harvested early after PC treatment with high concentrations of Ca and Thr or later after PC treatment with low Ca and Thr concentrations. Additional research aiming to measure the effects of Ca and Thr on bone formation in vivo is needed.

  • Effects of calcium and thrombin on growth factor release from platelet concentrates: Kinetics and regulation of Endothelial Cell Proliferation
    Biomaterials, 2004
    Co-Authors: I. Martineau, E Lacoste, G. Gagnon
    Abstract:

    Platelet concentrates (PCs) constitute new biological mediators used in osseous reconstructive surgery. In this study, we assessed (i) the effects of various concentrations of calcium and thrombin on the kinetics of platelet-derived growth factor (PDGF-BB), transforming growth factor-beta1(TGF-β1), basic fibroblast growth factor (bFGF), and vascular Endothelial growth factor (VEGF) release by PCs and (ii) the contribution of PC supernatants to Endothelial Cell Proliferation. Our results indicate that high concentrations of calcium (Ca) and thrombin (Thr) trigger an immediate and significant increase in bFGF, TGF-β1 and PDGF-BB concentrations. Thereafter, PDGF-BB, VEGF and TGF-β1 levels remained generally constant over a 6-day period while a decrease in bFGF concentrations was noted after 24h. Lower Ca and Thr concentrations tended to reduce and delay growth factors release from PCs. Endothelial Cell Proliferation was greatly enhanced with PC supernatants (mean: 20-fold increase). This was especially evident when Endothelial Cells were treated with supernatants harvested early after PC treatment with high concentrations of Ca and Thr or later after PC treatment with low Ca and Thr concentrations. Additional research aiming to measure the effects of Ca and Thr on bone formation in vivo is needed. © 2003 Elsevier Ltd. All rights reserved.

Richard Kendall - One of the best experts on this subject based on the ideXlab platform.

Karen K. Hirschi - One of the best experts on this subject based on the ideXlab platform.

  • Red light, green light: signals that control Endothelial Cell Proliferation during embryonic vascular development.
    Cell Cycle, 2004
    Co-Authors: Brenda L. Bohnsack, Karen K. Hirschi
    Abstract:

    : The proper regulation of Endothelial Cell Proliferation is critical for vascular development in the embryo. VEGF-A and bFGF, which are important in the induction of mesodermal progenitors to form a capillary plexus, are also key mitogenic signals. Disruption in VEGF-A or bFGF decreases Endothelial Cell Proliferation and halts vascular development. While stimulation of Endothelial Cell Proliferation is necessary during vasculogenesis, inhibitory signals such as TGF-beta1 and retinoic acid are equally important and required to inhibit Endothelial Cell Proliferation. These signals and activation of numerous downstream pathways must be properly integrated with extraCellular matrix proteins and integrin receptor signaling in order to form the embryonic vasculature. This coordination of mitogenic and anti-proliferative signals needed to form a circulatory network in the embryo may be unique relative to neovascularization in adult tissues where mitogenic stimulation promotes Proliferation of previously quiescent Endothelial Cells to repair and expand existing vasculature.

  • retinoic acid regulates Endothelial Cell Proliferation during vasculogenesis
    Development, 2003
    Co-Authors: Brenda L. Bohnsack, Karen Niederreither, Karen K. Hirschi
    Abstract:

    A dietary deficiency of vitamin A is associated with cardiovascular abnormalities in avian and murine systems. Retinoic acid (RA) is the active metabolite of vitamin A and whether it directly regulates mammalian blood vessel formation has not been determined and is investigated herein. We used mice rendered RA-deficient via targeted deletion of retinaldehyde dehydrogenase 2 ( Raldh2 -/- ), the enzyme required to produce active RA in the embryo. Histological examination at E8.0-8.5, prior to cardiac function and systemic blood circulation, revealed that capillary plexi formed in Raldh2 -/- yolk sacs and embryos, but were dilated, and not appropriately remodeled or patterned. Raldh2 -/- Endothelial Cells exhibited significantly increased expression of phosphohistone 3 and decreased expression of p21 and p27, suggesting that RA is required to control Endothelial Cell cycle progression during early vascular development. Uncontrolled Endothelial Cell growth, in Raldh2 -/- mutants, was associated with decreased Endothelial Cell maturation, disrupted vascular plexus remodeling and lack of later stages of vessel assembly, including mural Cell differentiation. Maternally administrated RA restored Endothelial Cell cycle control and vascular patterning. Thus, these data indicate that RA plays a crucial role in mammalian vascular development; it is required to control Endothelial Cell Proliferation and vascular remodeling during vasculogenesis.