Aortic Endothelial Cell

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Eugene A Sprague - One of the best experts on this subject based on the ideXlab platform.

  • Human Aortic Endothelial Cell response to 316L stainless steel material microstructure
    Journal of Materials Science: Materials in Medicine, 2009
    Co-Authors: Animesh Choubey, Denes Marton, Eugene A Sprague
    Abstract:

    The role of metal microstructure (e.g. grain sizes) in modulating Cell adherence behavior is not well understood. This study investigates the effect of varying grain sizes of 316L stainless steel (SS) on the attachment and spreading of human Aortic Endothelial Cells (HAECs). Four different grain size samples; from 16 to 66 μm (ASTM 9.0-4.9) were sectioned from sheets. Grain structure was revealed by polishing and etching with glycergia. Contact angle measurement was done to assess the hydrophilicity of the specimens. Atomic force microscopy (AFM) and X-ray photoelectron spectroscopy (XPS) were used to characterize the roughness and surface chemistry of the specimens. Cells were seeded on mechanically polished and chemically etched specimens followed by identification of activated focal adhesion sites using fluorescently tagged anti-pFAK (phosphorylated focal adhesion kinase). The 16 μm grain size etched specimens had significantly ( P  

  • Human Aortic Endothelial Cell response to 316L stainless steel material microstructure
    Journal of Materials Science: Materials in Medicine, 2009
    Co-Authors: Animesh Choubey, Denes Marton, Eugene A Sprague
    Abstract:

    The role of metal microstructure (e.g. grain sizes) in modulating Cell adherence behavior is not well understood. This study investigates the effect of varying grain sizes of 316L stainless steel (SS) on the attachment and spreading of human Aortic Endothelial Cells (HAECs). Four different grain size samples; from 16 to 66 μm (ASTM 9.0-4.9) were sectioned from sheets. Grain structure was revealed by polishing and etching with glycergia. Contact angle measurement was done to assess the hydrophilicity of the specimens. Atomic force microscopy (AFM) and X-ray photoelectron spectroscopy (XPS) were used to characterize the roughness and surface chemistry of the specimens. Cells were seeded on mechanically polished and chemically etched specimens followed by identification of activated focal adhesion sites using fluorescently tagged anti-pFAK (phosphorylated focal adhesion kinase). The 16 μm grain size etched specimens had significantly (P < 0.01) higher number of Cells attached per cm2 than other specimens, which may be attributed to the greater grain boundary area and associated higher surface free energy. This study shows that the underlying material microstructure may influence the HAEC behavior and may have important implications in Endothelialization.

  • human Aortic Endothelial Cell migration onto stent surfaces under static and flow conditions
    Journal of Vascular and Interventional Radiology, 1997
    Co-Authors: Eugene A Sprague, Jian Luo, Julio C Palmaz
    Abstract:

    Purpose The objective of the present study is to establish an in vitro model designed to quantitatively define human Aortic Endothelial Cell (HAEC) migration onto stainless steel stent material under both static and flow conditions of high and low wall shear stress. Materials and Methods To simulate implantation of a stent onto the intact arterial wall, HAECs were seeded and grown to confluence on thick, firm collagen gels. Flat 1 × 1-cm square, stainless steel pieces were implanted on this Endothelialized surface and migration of HAECs onto the steel surface was monitored, measured, and compared under static and high (15 dynes/cm 2 ) and low (2 dynes/cm 2 ) wall shear stress flow conditions designed to model wall shear stress levels encountered at different sites within the human arterial system. Results Under no flow, Endothelial Cell migration occurred uniformly from the periphery, attaining complete confluence over the square surface within 14 days. The initial migratory rate was approximately 10 (μm/h ± 0.5 on days 1–3 and increased to a rate near 15 μm/h ± 0.5 between days 10 and 14. High shear stress significantly ( P Conclusions These results indicate the rate and extent of Endothelial migration onto a prosthetic material surface are influenced by the level and direction of flow-related wall shear stress. Furthermore, these results demonstrate an in vitro model that provides a method to quantitatively evaluate and possibly predict the relative ability of different prosthetic materials to Endothelialize under variable in vivo flow conditions.

Naoki Mochizuki - One of the best experts on this subject based on the ideXlab platform.

  • selective inhibition of vascular Endothelial growth factor receptor 2 vegfr 2 identifies a central role for vegfr 2 in human Aortic Endothelial Cell responses to vegf
    Journal of Receptors and Signal Transduction, 2003
    Co-Authors: Akira Endo, Shigetomo Fukuhara, Michitaka Masuda, Toyonori Ohmori, Naoki Mochizuki
    Abstract:

    AbstractVascular Endothelial growth factor receptors (VEGFR) are considered essential for angiogenesis. The VEGFR‐family proteins consist of VEGFR‐1/Flt‐1, VEGFR‐2/KDR/Flk‐1, and VEGFR‐3/Flt‐4. Among these, VEGFR‐2 is thought to be principally responsible for angiogenesis. However, the precise role of VEGFRs1–3 in Endothelial Cell biology and angiogenesis remains unclear due in part to the lack of VEGFR‐specific inhibitors. We used the newly described, highly selective anilinoquinazoline inhibitor of VEGFR‐2 tyrosine kinase, ZM323881 (5‐[[7‐(benzyloxy) quinazolin‐4‐yl]amino]‐4‐fluoro‐2‐methylphenol), to explore the role of VEGFR‐2 in Endothelial Cell function. Consistent with its reported effects on VEGFR‐2 [IC(50) < 2 nM], ZM323881 inhibited activation of VEGFR‐2, but not of VEGFR‐1, epidermal growth factor receptor (EGFR), platelet‐derived growth factor receptor (PDGFR), or hepatocyte growth factor (HGF) receptor. We studied the effects of VEGF on human Aortic Endothelial Cells (HAECs), which express VE...

Animesh Choubey - One of the best experts on this subject based on the ideXlab platform.

  • Human Aortic Endothelial Cell response to 316L stainless steel material microstructure
    Journal of Materials Science: Materials in Medicine, 2009
    Co-Authors: Animesh Choubey, Denes Marton, Eugene A Sprague
    Abstract:

    The role of metal microstructure (e.g. grain sizes) in modulating Cell adherence behavior is not well understood. This study investigates the effect of varying grain sizes of 316L stainless steel (SS) on the attachment and spreading of human Aortic Endothelial Cells (HAECs). Four different grain size samples; from 16 to 66 μm (ASTM 9.0-4.9) were sectioned from sheets. Grain structure was revealed by polishing and etching with glycergia. Contact angle measurement was done to assess the hydrophilicity of the specimens. Atomic force microscopy (AFM) and X-ray photoelectron spectroscopy (XPS) were used to characterize the roughness and surface chemistry of the specimens. Cells were seeded on mechanically polished and chemically etched specimens followed by identification of activated focal adhesion sites using fluorescently tagged anti-pFAK (phosphorylated focal adhesion kinase). The 16 μm grain size etched specimens had significantly ( P  

  • Human Aortic Endothelial Cell response to 316L stainless steel material microstructure
    Journal of Materials Science: Materials in Medicine, 2009
    Co-Authors: Animesh Choubey, Denes Marton, Eugene A Sprague
    Abstract:

    The role of metal microstructure (e.g. grain sizes) in modulating Cell adherence behavior is not well understood. This study investigates the effect of varying grain sizes of 316L stainless steel (SS) on the attachment and spreading of human Aortic Endothelial Cells (HAECs). Four different grain size samples; from 16 to 66 μm (ASTM 9.0-4.9) were sectioned from sheets. Grain structure was revealed by polishing and etching with glycergia. Contact angle measurement was done to assess the hydrophilicity of the specimens. Atomic force microscopy (AFM) and X-ray photoelectron spectroscopy (XPS) were used to characterize the roughness and surface chemistry of the specimens. Cells were seeded on mechanically polished and chemically etched specimens followed by identification of activated focal adhesion sites using fluorescently tagged anti-pFAK (phosphorylated focal adhesion kinase). The 16 μm grain size etched specimens had significantly (P < 0.01) higher number of Cells attached per cm2 than other specimens, which may be attributed to the greater grain boundary area and associated higher surface free energy. This study shows that the underlying material microstructure may influence the HAEC behavior and may have important implications in Endothelialization.

Morsen Meydani - One of the best experts on this subject based on the ideXlab platform.

  • effect of vitamin e on human Aortic Endothelial Cell production of chemokines and adhesion to monocytes
    Atherosclerosis, 1999
    Co-Authors: Takuro Koga, Keith R Martin, Morsen Meydani
    Abstract:

    Epidemiological and clinical studies indicate that vitamin E may reduce the risk of cardiovascular disease (CVD). Modulation of adhesion molecule expression and chemokine production by vitamin E may contribute to its beneficial effect. In this study we found that the enrichment of confluent human Aortic Endothelial Cells (HAEC) or U937 monocytic Cells with increasing doses of vitamin E (d-alpha-tocopherol, 20, 40, and 60 micromol/l for 20 h) inhibited their adhesion when either or both Cell types were stimulated with interleukin (IL)-1beta. Enrichment of HAEC with the same doses of vitamin E suppressed IL-1beta-stimulated expression of interCellular adhesion molecule-1 (ICAM-1), vascular Cell adhesion molecule-1 (VCAM-1), and Endothelial leukocyte adhesion molecule-1 (E-selectin). Supplementation with increasing doses of vitamin E up to 60 micromol/l was not effective in preventing spontaneous production of monocyte chemoattractant protein-1 (MCP-1), but supplementation with vitamin E at 60 micromol/l reduced IL-8 production significantly. However, IL-1beta-induced productions of both MCP-1 and IL-8 were dose-dependently suppressed by enrichment of Cells with vitamin E. Vitamin E, at the doses used, did not significantly change the spontaneous production but dose-dependently inhibited the IL-1beta-induced production of inflammatory cytokine IL-6. We concluded that vitamin E could inhibit production of chemokines and inflammatory cytokines, in addition to inhibiting adhesion of HAEC to monocytes by reducing expression of adhesion molecules when Cells were activated with an inflammatory cytokine. These mediators are actively involved in the pathogenesis of atherosclerosis. Therefore, their inhibition by vitamin E may contribute to vitamin E's reported reduction in risk of CVD.

  • effect of vitamin e on human Aortic Endothelial Cell responses to oxidative injury
    Free Radical Biology and Medicine, 1996
    Co-Authors: Antonio Martin, Wendy Baur, Simin Nikbin Meydani, Jeffrey B Blumberg, Morsen Meydani
    Abstract:

    Abstract Reactive oxygen species produced by the Cells present in the arterial wall may cause oxidative damage to Cellular components altering Endothelial Cell (EC) function. Changes in the EC function appear to play a key role in the pathogenesis of atherosclerosis. Human Aortic Endothelial Cells (HAEC) were employed to investigate the protective role of vitamin E upon exposure of Endothelial Cells to oxidative stress in vitro. HAEC assimilate d-α-tocopherol from the media in a dose-dependent manner. Exposure of HAEC to 16.5 mM of the free radical generator 2,2'-azobis (2-amidinopropane) hydrochloride (AAPH) for 16 h decreased Cell viability (assessed by trypan blue exclusion) from 90 to 28%. HAEC preincubated with vitamin E at 15, 30, and 60 pM prior to the AAPH exposure resulted in a dose-dependent increase in resistance to oxidative stress and increased Cell viability by 37, 66, and 85%, respectively. An increase in prostacyclin (PGI2) production by HAEC in response to AAPH exposure was correlated positively with Cell damage and negatively with vitamin E concentration. Interleukin (IL)-1 production also increased in parallel with Cell damage induced by AAPH. Vitamin E treatment significantly reduced IL-1 production after AAPH exposure. This modulatory role of vitamin E on HAEC function following exposure to an oxidative stress may reflect its antioxidant protection against lipid peroxidation.

Scott L Stevens - One of the best experts on this subject based on the ideXlab platform.

  • vascular Endothelial growth factor and heparin in a biologic glue promotes human Aortic Endothelial Cell proliferation with Aortic smooth muscle Cell inhibition
    Surgery, 1996
    Co-Authors: David A Weatherford, Jill E Sackman, Tonya T Reddick, Michael B Freeman, Scott L Stevens
    Abstract:

    Background . Incomplete luminal Endothelialization may contribute to small diameter vascular graft failure. Vascular Endothelial growth factor (VEGF) can be used to stimulate Endothelialization without provoking smooth muscle Cell (SMC) proliferation. Heparin and VEGF in a fibrin glue (FG) were investigated for their ability to promote selective human Aortic Endothelial Cell (HAEC) proliferation and human Aortic smooth muscle Cell (HASMC) inhibition. Methods . HAECs and HASMCs were seeded on FG containing VEGF (2.5, 10, 30, 100 ng/ml) or VEGF and heparin (5, 50, 500 units/ml). Proliferation assays were performed with tritiated thymidine on days 1 and 3. Results were analyzed by ANOVA, with p≤0.05 significant. Results . HAEC proliferation on FG with 10, 30, and 100 ng/ml VEGF was significantly greater than FG alone at days 1 and 3. The addition of 50 units/ml heparin to VEGF significantly increased HAEC proliferation to greater than FG with VEGF alone at day 1. Human Aortic SMC proliferation was not stimulated by the addition of VEGF. The addition of 5, 50, and 500 units/ml heparin significantly inhibited HASMC proliferation regardless of VEGF concentration. Discussion . VEGF at 10 ng/ml combined with heparin at 50 units/ml exhibited maximal stimulation of HAECs with inhibition of HASMCs. VEGF and heparin in a biologic glue may improve patency by selectively promoting HAEC proliferation without HASMC growth on synthetic vascular bypass grafts.