Role of laminin and basement membrane in the morphological differentiation of human endothelial cells into capillary-like structures.

Kubota, Yasuo; Kleinman, Hynda K.; Martin, George R.; Lawley, Thomas J.

doi:10.1083/jcb.107.4.1589

Cited by 1,114 publications

(703 citation statements)

References 18 publications

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“…These functions are essential steps for neovessel sprouting (Kubota et al, 1988;Connolly et al, 1989) and angiogenesis, which is an important biological process involved in metastasis formation (Liotta et al, 1991;Weidner et al, 1991). Importantly, throughout the experiment with the CAM model, this study showed NAMI-A to prevent in vivo angiogenesis at doses known to have anti-metastasis activity.…”

Section: Discussionmentioning

confidence: 62%

Inhibition of endothelial cell functions and of angiogenesis by the metastasis inhibitor NAMI-A

et al. 2002

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NAMI-A is a ruthenium-based compound with selective anti-metastasis activity in experimental models of solid tumours. We studied whether this activity was dependent on anti-angiogenic ability of NAMI-A. We thus investigated its in vitro effects on endothelial cell functions necessary for angiogenesis to develop, as well as its in vivo effects in the chick embryo chorioallantoic membrane model. Endothelial cell proliferation, chemotaxis, and secretion of the matrix-degrading enzyme metalloproteinase-2 were inhibited by NAMI-A in a dose-dependent manner, and without morphologic signs of cell apoptosis or necrosis. Lastly, NAMI-A displayed a dose-dependent in vivo anti-angiogenic activity in the chorioallantoic membrane model. These data suggest that the anti-angiogenic activity of NAMI-A can contribute to its anti-metastatic efficacy in mice bearing malignant solid tumours.

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Section: Discussionmentioning

confidence: 62%

Inhibition of endothelial cell functions and of angiogenesis by the metastasis inhibitor NAMI-A

et al. 2002

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“…Matrigel (0.5 ml at a concentration of 10-12 mg/ml) was pipetted into 13-mm-diameter tissue culture wells and polymerized at 37°C for 30 minutes to 1 hour (15,16). MSCs and EL-MSCs from SSc patients and controls were plated (6 ϫ 10 4 cells/ml) in IMDM with 1% FBS.…”

Section: Methodsmentioning

confidence: 99%

Impairment of endothelial cell differentiation from bone marrow–derived mesenchymal stem cells: New insight into the pathogenesis of systemic sclerosis

Cipriani

Guiducci

Miniati

et al. 2007

Arthritis & Rheumatism

146

102

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Objective. Systemic sclerosis (SSc) is a disorder characterized by vascular damage and fibrosis of the skin and internal organs. Despite marked tissue hypoxia, there is no evidence of compensatory angiogenesis. The ability of mesenchymal stem cells (MSCs) to differentiate into endothelial cells was recently demonstrated. The aim of this study was to determine whether impaired differentiation of MSCs into endothelial cells in SSc might contribute to disease pathogenesis by decreasing endothelial repair.Methods. MSCs obtained from 7 SSc patients and 15 healthy controls were characterized. The number of colony-forming unit-fibroblastoid colonies was determined. After culture in endothelial-specific medium, the endothelial-like MSC (EL-MSC) phenotype was assessed according to the surface expression of vascular endothelial growth factor receptors (VEGFRs). Senescence, chemoinvasion, and capillary morphogenesis studies were also performed.Results. MSCs from SSc patients displayed the same phenotype and clonogenic activity as those from controls. In SSc MSCs, a decreased percentage of VEGFR-2؉, CXCR4؉, VEGFR-2؉/CXCR4؉ cells and early senescence was detected. After culturing, SSc EL-MSCs showed increased expression of VEGFR-1, VEGFR-2, and CXCR4, did not express CD31 or annexin V, and showed significantly decreased migration after specific stimuli. Moreover, the addition of VEGF and stromal cell-derived factor 1 to cultured SSc ELMSCs increased their angiogenic potential less than that in controls.Conclusion. Our data strongly suggest that endothelial repair may be affected in SSc. The possibility that endothelial progenitor cells could be used to increase vessel growth in chronic ischemic tissues may open up new avenues in the treatment of vascular damage caused by SSc.

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“…Moreover, high titers of AECA in patients with SLE are associated with an active lesion of the kidney and vasculitis, and it has therefore been suggested that the AECA titer could be used as a measure of renal involvement (16). Microvascular endothelial cells carry a specific antigen profile that is quite different from the profiles of the large vessels (17,18). In BD, vasculitis mainly involves capillaries and small vessels (2,3).…”

Section: Aeca Against ␣-Enolase In Behç Et's Disease 2031mentioning

confidence: 99%

Human α‐enolase from endothelial cells as a target antigen of anti–endothelial cell antibody in Behçet's disease

Lee¹,

Chung²,

Kim³

et al. 2003

Arthritis & Rheumatism

174

108

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Objective. To identify and recombine a protein of the human dermal microvascular endothelial cell (HD-MEC) that specifically reacts with anti-endothelial cell antibody (AECA) in the serum of patients with Behçet's disease (BD), and to evaluate the usefulness of this protein in BD.Methods. The proteomics technique, with 2-dimensional gel electrophoresis and matrix-assisted laser desorption ionization؊time-of-flight (MALDI-TOF) mass spectrometry, was used to identify and recombine HDMEC antigen. Western blotting and enzyme-linked immunosorbent assay (ELISA) of recombinant protein isolated by gene cloning were performed on serum from healthy controls, patients with BD, and patients with other rheumatic diseases (rheumatoid arthritis, systemic lupus erythematosus, and Wegener's granulomatosis).Results. Eighteen of 40 BD patients had serum IgM antibody to HDMEC antigen. The purified protein that reacted with AECA in BD patient sera was found to be ␣-enolase by 2-dimensional gel electrophoresis followed by immunoblotting and MALDI-TOF mass spectrometry. Recombinant ␣-enolase protein was isolated and refined by gene cloning. On Western blots, AECApositive IgM from the sera of patients with active BD reacted strongly with recombinant human ␣-enolase. BD patient sera positive for anti-␣-enolase did not react with human ␥-enolase. On dot-blotting, reactivity to human ␣-enolase was detected only in the IgM-positive group. Fifteen of the 18 AECA-positive sera that were positive for the HDMEC antigen showed reactivity to recombinant ␣-enolase IgM antibody by ELISA.Conclusion. The ␣-enolase protein is the target protein of serum AECA in BD patients. This is the first report of the presence of IgM antibodies to ␣-enolase in endothelial cells from the serum of BD patients. Although further studies relating this protein to the pathogenesis of BD will be necessary, ␣-enolase and its antibody may prove useful in the development of new diagnostic and treatment modalities in BD.

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Role of laminin and basement membrane in the morphological differentiation of human endothelial cells into capillary-like structures.

Cited by 1,114 publications

References 18 publications

Inhibition of endothelial cell functions and of angiogenesis by the metastasis inhibitor NAMI-A

Inhibition of endothelial cell functions and of angiogenesis by the metastasis inhibitor NAMI-A

Impairment of endothelial cell differentiation from bone marrow–derived mesenchymal stem cells: New insight into the pathogenesis of systemic sclerosis

Human α‐enolase from endothelial cells as a target antigen of anti–endothelial cell antibody in Behçet's disease

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