Vascular endothelial growth factor receptors in the regulation of angiogenesis and lymphangiogenesis

Karkkainen, Marika J.; Petrova, Tatiana V.

doi:10.1038/sj.onc.1203855

Cited by 389 publications

(276 citation statements)

References 82 publications

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“…6,7 VEGF acts by interacting with a family of specific receptor tyrosine kinases that includes VEGF receptor (R)-1 (flt-1), VEGFR-2 (flk-1/kinase insert domain receptor [KDR]), and VEGFR-3/flt-4. 8 Disruption of VEGFRs interferes with differentiation of endothelial cells, and it is lethal for the embryo. Endothelial cells express all 3 different VEGFRs.…”

mentioning

confidence: 99%

Expression of Vascular Endothelial Growth Factor Receptor-2 or Tie-2 on Peripheral Blood Cells Defines Functionally Competent Cell Populations Capable of Reendothelialization

et al. 2004

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Background— Receptor tyrosine kinases that include vascular endothelial growth factor (VEGFR)-1, VEGFR-2, and Tie-2 regulate cardiovascular development and physiological and pathological angiogenesis. We were interested in the phenotypic and functional characterization of peripheral blood cells expressing these receptors and their therapeutic potential in vascular injury. Methods and Results— VEGFR-1 + , VEGFR-2 + , and Tie-2 + cells constituted ≈3.0±0.2%, 0.8±0.5%, and 2.0±0.3%, respectively, of the total population of mononuclear cells in blood. Phenotypic analysis demonstrated that all 3 cell populations mainly expressed markers of monocytic/macrophage lineage. Only VEGFR-2 + and Tie-2 + cells phenotypically, morphologically, and functionally differentiated to endothelial cells after culture, whereas VEGFR-1 + cells did not. None of the cell types proliferated in vitro. Only freshly isolated VEGFR-2 + or Tie-2 + cells but not VEGFR-2 − or Tie-2 − cell populations significantly contributed to efficient endothelialization of balloon-injured femoral arteries of nude mice. Furthermore, these cells also differentiated into α-actin–positive smooth muscle cells. Administration of bromodeoxyuridine to animals transplanted with human endothelial progenitor cells showed that VEGFR-2 + and Tie-2 + cells proliferated in vivo. Conclusions— These data demonstrate that expression of VEGFR-2 and/or Tie-2 on peripheral blood cells defines functionally competent cell populations that proliferate in vivo and that contribute to reendothelialization. These findings may have implications for a cell-based approach in vascular diseases.

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confidence: 99%

Expression of Vascular Endothelial Growth Factor Receptor-2 or Tie-2 on Peripheral Blood Cells Defines Functionally Competent Cell Populations Capable of Reendothelialization

et al. 2004

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“…3 -5 For example, the extent of neovascularization in primary tumors has been shown to correlate with a negative prognosis in small cell lung carcinoma, prostate, and breast cancers. 6 A number of positive and negative cytokine mediators of tumor angiogenesis have been described, including transforming growth factor beta (TGF -), 7,8 vascular endothelial growth factor (VEGF ), 9,10 fibroblast growth factor ( FGF ), 11 interferon-, 3 and thrombospondin (TSP -1 ). 2 The tumor-suppressor gene p53 has been shown to transcriptionally regulate a number of factors, some of which are secreted proteins that either inhibit (e.g., glioblastoma-derived angiogenesis inhibiting factor ( GD -AIF ) and TSP -1) or promote (e.g., VEGF and FGF ) angiogenesis.…”

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confidence: 99%

Downmodulation of bFGF-binding protein expression following restoration of p53 function

et al. 2001

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Angiogenesis is a requirement for solid tumor growth. Therefore, inhibition of this neovascularization is one mechanism by which restoration of wtp53 function may lead to tumor regression. Here we report that adenoviral vector -mediated wild -type p53 transduction results in growth inhibition of squamous cell carcinoma of the head and neck tumor cells both in vitro and in a xenograft mouse model. This growth inhibition is associated with the down -regulation of the expression of fibroblast growth factor binding protein, a secreted protein required for the activation of angiogenic factor basic FGF. These findings suggest that wtp53 -induced tumor regression is due, at least in part, to antiangiogenesis mediated by the downmodulation of fibroblast growth factor binding protein. Cancer Gene Therapy ( 2001 ) 8, 771 -782

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“…3 In mammals, there are six members of the VEGF family: VEGF, VEGF-B, VEGF-C, VEGF-D, VEGF-E, and placenta growth factor (PlGF). 4,5 Three types of tyrosine kinase receptors (VEGF receptor-1 [VEGFR-1], VEGFR-2, and VEGFR-3) have been reported as specific receptors for the VEGF family. 4,5 VEGF-C and VEGF-D have been identified as specific lymphangiogenic factors, which bind to and induce phosphorylation of VEGFR-3.…”

Section: Introductionmentioning

confidence: 99%

“…4,5 Three types of tyrosine kinase receptors (VEGF receptor-1 [VEGFR-1], VEGFR-2, and VEGFR-3) have been reported as specific receptors for the VEGF family. 4,5 VEGF-C and VEGF-D have been identified as specific lymphangiogenic factors, which bind to and induce phosphorylation of VEGFR-3. 6 -8 These factors stimulate lymphangiogenesis in vivo, for example, in the avian chorioallantoic membrane and in the skin of transgenic mice.…”

Section: Introductionmentioning

confidence: 99%

Clinical significance of vascular endothelial growth factor‐C and vascular endothelial growth factor receptor 3 in patients with T1 lung adenocarcinoma

Kojima

Shijubo

Yamada

et al. 2005

Cancer

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The weight of characters is a crucial step in different population analyses. We propose a new formula to facilitate this while establishing a scale that follows the criteria of the probability of change in each character. This method is described for drawing of median‐joining networks, yet it could also be used for other methods in which the weight of the characters is required. Am J Phys Anthropol, 2010. © 2010 Wiley‐Liss, Inc.

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Vascular endothelial growth factor receptors in the regulation of angiogenesis and lymphangiogenesis

Cited by 389 publications

References 82 publications

Expression of Vascular Endothelial Growth Factor Receptor-2 or Tie-2 on Peripheral Blood Cells Defines Functionally Competent Cell Populations Capable of Reendothelialization

Expression of Vascular Endothelial Growth Factor Receptor-2 or Tie-2 on Peripheral Blood Cells Defines Functionally Competent Cell Populations Capable of Reendothelialization

Downmodulation of bFGF-binding protein expression following restoration of p53 function

Clinical significance of vascular endothelial growth factor‐C and vascular endothelial growth factor receptor 3 in patients with T1 lung adenocarcinoma

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