Intrinsic pro-angiogenic status of cystic fibrosis airway epithelial cells

Verhaeghe, Catherine; Tabruyn, Sébastien P.; Oury, Cécile

doi:10.1016/j.bbrc.2007.02.166

Cited by 25 publications

(22 citation statements)

References 26 publications

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“…Our conclusion that CFTR dysfunction triggers VEGF-A synthesis is based on data obtained in cultured airway epithelial cells. Previously, VERHAEGHE et al [30] reported increased VEGF-A synthesis in a human fetal cell line carrying the homozygous mutation F508del compared with a control human fetal cell line. These latter data provided circumstantial evidence of a role for CFTR dysfunction in VEGF-A production; however, differences between these two cell lines could have been unrelated to CFTR dysfunction [31].…”

Section: Discussionmentioning

confidence: 99%

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CFTR dysfunction induces vascular endothelial growth factor synthesis in airway epithelium

Martin

Coolen

et al. 2013

Eur Respir J

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Section: Discussionmentioning

confidence: 99%

“…Increased VEGF-A synthesis in airway epithelium could contribute to angiogenesis [11,30] and increase in vascular permeability, facilitating recruitment of inflammatory cells (e.g. neutrophils) and proteins in the airways.…”

Section: Discussionmentioning

confidence: 99%

CFTR dysfunction induces vascular endothelial growth factor synthesis in airway epithelium

Martin

Coolen

et al. 2013

Eur Respir J

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“…Human umbilical vein endothelial cells (HUVEC) were isolated and cultured as described previously (20). Cells between passages 1 and 3 were used for experiments.…”

Section: Cell Cultures and Reagentsmentioning

confidence: 99%

“…Sprouting Assay Sprouting assays were carried on as described previously (20). HUVECs were suspended in culture medium and seeded on nonadherent plates.…”

Section: Cell Cultures and Reagentsmentioning

confidence: 99%

NF-κB activation in endothelial cells is critical for the activity of angiostatic agents

Tabruyn

Mémet

Avé

et al. 2009

Molecular Cancer Therapeutics

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In tumor cells, the transcription factor NF-κB has been described to be antiapoptotic and proproliferative and involved in the production of angiogenic factors such as vascular endothelial growth factor. From these data, a protumorigenic role of NF-κB has emerged. Here, we examined in endothelial cells whether NF-κB signaling pathway is involved in mediating the angiostatic properties of angiogenesis inhibitors. The current report describes that biochemically unrelated agents with direct angiostatic effect induced NF-κB activation in endothelial cells. Our data showed that endostatin, anginex, angiostatin, and the 16-kDa N-terminal fragment of human prolactin induced NF-κB activation in endothelial cells in both cultured human endothelial cells and in vivo in a mouse tumor model. It was also found that NF-κB activity was required for the angiostatic activity, because inhibition of NF-κB in endothelial cells impaired the ability of angiostatic agents to block sprouting of endothelial cells and to overcome endothelial cell anergy. Therefore, activation of NF-κB in endothelial cells can result in an unexpected antitumor outcome. Based on these data, the current approach of systemic treatment with NF-κB inhibitors may therefore be revisited because NF-κB activation specifically targeted to endothelial cells might represent an efficient strategy for the treatment of cancer. [Mol Cancer Ther 2009;8(9):2645-54]

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“…The production of VEGF, and the induction of angiogenesis, is commonly interpreted as a consequence of the inflammation process. Importantly, Verhaeghe et al (37) reported that local overproduction of proangiogenic factors in CF fetal human tracheal epithelial cells was sufficient to stimulate angiogenesis. Their results suggest that the intrin-sic proangiogenic status of the CF respiratory epithelial cells contributes to the development of lung angiogenesis.…”

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confidence: 99%

EG-VEGF, BV8, and their receptor expression in human bronchi and their modification in cystic fibrosis: Impact of CFTR mutation (delF508)

Chauvet

Traboulsi

Thevenon

et al. 2015

American Journal of Physiology-Lung Cellular and Molecular Phys

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Enhanced lung angiogenesis has been reported in cystic fibrosis (CF). Recently, two highly homologous ligands, endocrine gland vascular endothelial growth factor (EG-VEGF) and mammalian Bv8, have been described as new angiogenic factors. Both ligands bind and activate two closely related G protein-coupled receptors, the prokineticin receptor (PROKR) 1 and 2. Yet, the expression, regulation, and potential role of EG-VEGF, BV8, and their receptors in normal and CF lung are still unknown. The expression of the receptors and their ligands was examined using molecular, biochemical, and immunocytochemistry analyses in lungs obtained from CF patients vs. control and in normal and CF bronchial epithelial cells. Cystic fibrosis transmembrane conductance regulator (CFTR) activity was evaluated in relation to both ligands, and concentrations of EG-VEGF were measured by ELISA. At the mRNA level, EG-VEGF, BV8, and PROKR2 gene expression was, respectively, approximately five, four, and two times higher in CF lungs compared with the controls. At the cellular level, both the ligands and their receptors showed elevated expressions in the CF condition. Similar results were observed at the protein level. The EG-VEGF secretion was apical and was approximately two times higher in CF compared with the normal epithelial cells. This secretion was increased following the inhibition of CFTR chloride channel activity. More importantly, EG-VEGF and BV8 increased the intracellular concentration of Ca2+ and cAMP and stimulated CFTR-chloride channel activity. Altogether, these data suggest local roles for epithelial BV8 and EG-VEGF in the CF airway peribronchial vascular remodeling and highlighted the role of CFTR activity in both ligand biosynthesis and secretion.

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Intrinsic pro-angiogenic status of cystic fibrosis airway epithelial cells

Cited by 25 publications

References 26 publications

CFTR dysfunction induces vascular endothelial growth factor synthesis in airway epithelium

CFTR dysfunction induces vascular endothelial growth factor synthesis in airway epithelium

NF-κB activation in endothelial cells is critical for the activity of angiostatic agents

EG-VEGF, BV8, and their receptor expression in human bronchi and their modification in cystic fibrosis: Impact of CFTR mutation (delF508)

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