Interaction of fibronectin with cultured human endothelial cells: characterization of the specific receptor

Conforti, G; Zanetti, Adriana; Colella, S; Abbadini, Marzia; Marchisio, Pier Carlo; Pytela, Robert; Giancotti, Filippo G.; Tarone, Guido; Languino, Lucia R.; Dejana, Elisabetta

doi:10.1182/blood.v73.6.1576.1576

Cited by 68 publications

(23 citation statements)

References 36 publications

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“…Both the a v b 3 and a 5 b 1 integrin are highly expressed in endothelial cells (66)(67)(68)(69). Although integrin surface densities have not been reported for HAEC, a 5 b 1 expression in HUVEC has been reported to be ;7.5 3 10 5 receptors per cell (68). The expression of a v b 3 and a 5 b 1 has been reported to be altered by shear stress.…”

Section: Discussionmentioning

confidence: 99%

Endothelial Cell Migration on RGD-Peptide-Containing PEG Hydrogels in the Presence of Sphingosine 1-Phosphate

Wacker

Alford

Scott

et al. 2008

Biophysical Journal

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Sphingosine 1-phosphate (S1P) is a potent chemokinetic agent for endothelial cells that is released by activated platelets. We previously developed Arg-Gly-Asp (RGD)-containing polyethylene glycol biomaterials for the controlled delivery of S1P to promote endothelialization. Here, we studied the effects of cell adhesion strength on S1P-stimulated endothelial cell migration in the presence of arterial levels of fluid shear stress, since an upward shift in optimal cell adhesion strengths may be beneficial for promoting long-term cell adhesion to materials. Two RGD peptides with different integrin-binding specificities were added to the polyethylene glycol hydrogels. A linear RGD bound primarily to beta(3) integrins, whereas a cyclic RGD bound through both beta(1) and beta(3) integrins. We observed increased focal adhesion formation and better long-term adhesion in flow with endothelial cells on linear RGD peptide, versus cyclic RGD, even though initial adhesion strengths were higher for cells on cyclic RGD. Addition of 100 nM S1P increased cell speed and random motility coefficients on both RGD peptides, with the largest increases found on cyclic RGD. For both peptides, much of the increase in cell migration speed was found for smaller cells (<1522 microm(2) projected area), although the large increases on cyclic RGD were also due to medium-sized cells (2288-3519 microm(2)). Overall, a compromise between high cell migration rates and long-term adhesion will be important in the design of materials that endothelialize after implantation.

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Section: Discussionmentioning

confidence: 99%

Endothelial Cell Migration on RGD-Peptide-Containing PEG Hydrogels in the Presence of Sphingosine 1-Phosphate

Wacker

Alford

Scott

et al. 2008

Biophysical Journal

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“…For binding studies, infected and uninfected HUVEC were detached as described by Conforti et al (5). The cells were treated for 30 s at 37°C with 1 ml of a prewarmed solution of 0.05% trypsin and 0.53 mM EDTA.…”

Section: Methodsmentioning

confidence: 99%

von Willebrand factor release and thrombomodulin and tissue factor expression in Rickettsia conorii-infected endothelial cells

et al. 1992

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Mediterranean spotted fever, a tick-borne rickettsiosis caused by Rickettsia conorii, may lead to small-vessel or deep-vein thrombosis. In order to evaluate the role of endothelial cell alteration in this lesion, we infected human endothelial cells derived from umbilical veins with R. conorii. We report the induction of two previously unreported prothrombotic mechanisms in rickettsial disease: (i) a progressive decline in thrombomodulin antigen and (ii) early expression of tissue factor, and, as described for R. rickettsii infection, later release of von Willebrand factor from Weibel-Palade bodies. Thrombomodulin expression in infected endothelial cells, measured by the thrombin-dependent activation of protein C or flow cytometric analysis, decreased steadily between 4 and 24 h after inoculation with rickettsiae. R. conorii infection induced tissue factor expression, measured by clotting assay and flow cytometric analysis, which was detectable 2 h postinoculation, reached its maximum 4 h postinoculation, and progressively decreased thereafter. Infection resulted in a relatively late release ofvon Willebrand factor antigen into the culture medium. A double-label immunofluorescence assay for the simultaneous evaluation of von Willebrand factor and R. conorii showed that the depletion of cytoplasmic von Willebrand factor stored in Weibel-Palade bodies was due to a direct effect of the intracellular R. conorii. These disturbances of endothelial function observed with R. conorii-infected cells may provide a paradigm for the elucidation of thrombotic pathobiology with Mediterranean spotted fever.

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“…A large number of integrins (α 1 β 1 , α 2 β 1 , α 3 β 1 , α 5 β 1 , and α 6 β 1 ) have been identified in endothelial cells (Hodivala‐Dilke et al, 2003; Mehta and Malik, 2006). The extracellular domain of integrins interacts with the Arg‐Gly‐Asp (RGD) domain of ECM proteins such as fibronectin, fibrinogen, vitronectin, and collagen (Conforti et al, 1989; Hynes, 1992; Hodivala‐Dilke et al, 2003).…”

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confidence: 99%

Impaired integrin‐mediated adhesion contributes to reduced barrier properties in VASP‐deficient microvascular endothelium

Schlegel

Waschke

2009

Journal Cellular Physiology

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Recent studies point to a significant role of vasodilator-stimulated phosphoprotein (VASP) in the maintenance of endothelial barrier functions in vivo and in vitro. Moreover, it has been reported that VASP is required for activation of the small GTPase Rac 1. However, little is known whether VASP is involved in the regulation of cell adhesion molecules that are critical for maintenance of the endothelial barrier. Here we demonstrate that impaired barrier properties in VASP-deficient (VASP-/-) microvascular myocardial endothelial cells (MyEnd) correlated with both impaired integrin-mediated adhesion as revealed by laser tweezer trapping and reduced integrin-dependent cell migration. This was paralleled by reduction of focal adhesions at the cell periphery as well as of beta(1)-integrin and VE-cadherin cytoskeletal anchorage. Incubation of MyEnd VASP wt with RGD peptide to block interaction of integrins with extracellular matrix (ECM) reduced barrier properties and Rac 1 activity in wt endothelial monolayers mimicking the situation in VASP (-/-) cells under resting conditions. Moreover, cAMP-mediated Rac 1 activation was reduced under conditions of impaired integrin-mediated adhesion in wt cells and cAMP-induced increase in VE-cadherin cytoskeletal anchorage was abolished in VASP (-/-) endothelium. In summary, these data indicate that VASP is required for integrin-mediated adhesion which stabilizes endothelial barrier properties at least in part by facilitating Rac 1 activation.

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Interaction of fibronectin with cultured human endothelial cells: characterization of the specific receptor

Cited by 68 publications

References 36 publications

Endothelial Cell Migration on RGD-Peptide-Containing PEG Hydrogels in the Presence of Sphingosine 1-Phosphate

Endothelial Cell Migration on RGD-Peptide-Containing PEG Hydrogels in the Presence of Sphingosine 1-Phosphate

von Willebrand factor release and thrombomodulin and tissue factor expression in Rickettsia conorii-infected endothelial cells

Impaired integrin‐mediated adhesion contributes to reduced barrier properties in VASP‐deficient microvascular endothelium

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