Angiogenesis in paediatric airway disease

Wilson, John W.; Robertson, Colin F.

doi:10.1016/s1526-0542(02)00200-2

Cited by 23 publications

(20 citation statements)

References 117 publications

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“…In both adults and children recent biopsy studies have demonstrated a large increase in the number of microvessels present in the airways of patients with chronic asthma, with some evidence that the endothelium of these vessels is undergoing proliferation (Vrugt et al 2000;Wilson & Robertson 2002;Barbato et al 2006). Vascular remodeling has also been shown to occur in a chronic allergen exposure rat model (Tigani et al 2006).…”

Section: Vascular Remodelingmentioning

confidence: 99%

Pathogenesis of Asthma

Holgate¹

2008

Clin Experimental Allergy

681

486

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While asthma is considered an inflammatory disorder of the conducting airways, it is becoming increasingly apparent that the disease is heterogeneous with respect to immunopathology, clinical phenotypes, response to therapies, and natural history. Once considered purely an allergic disorder dominated by Th2-type lymphocytes, IgE, mast cells, eosinophils, macrophages, and cytokines, the disease also involves local epithelial, mesenchymal, vascular and neurologic events that are involved in directing the Th2 phenotype to the lung and through aberrant injury-repair mechanisms to remodeling of the airway wall. Structural cells provide the necessary "soil" upon which the "seeds" of the inflammatory response are able to take root and maintain a chronic phenotype and upon which are superimposed acute and subacute episodes usually driven by environmental factors such as exposure to allergens, microorganisms, pollutants or caused by inadequate antiinflammatory treatment. Greater consideration of additional immunologic and inflammatory pathways are revealing new ways of intervening in the prevention and treatment of the disease. Thus increased focus on environmental factors beyond allergic exposure (such as virus infection, air pollution, and diet) are identifying targets in structural as well as immune and inflammatory cells at which to direct new interventions.

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Section: Vascular Remodelingmentioning

confidence: 99%

Pathogenesis of Asthma

Holgate¹

2008

Clin Experimental Allergy

681

486

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“…Inflammatory mediators and growth factors have the capacity to cause cell infiltration and epithelial injury and to increase bronchial vascularization. The latter is due to the activation of the angiogenic process, which contributes to increase the portal entry for inflammatory cells (40). The magnitude of the vascular remodeling is correlated to the degree of inflammation resulting from infection, since it is not observed, to such extent, in noninfective chronic inflammation (40).…”

mentioning

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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“…9,10 The remodeling and the pathogenesis of chronic pulmonary disorders may involve endothelial cells. 11,12 Thus, inhalation of ambient air particles have shown acute effects on endothelial cells. 13 The interaction between macrophages, epithelial and endothelial lung cells, and attracted leukocytes, involves the release of pro-inflammatory mediators, such as interleukin (IL)-1α and IL-1β, tumor necrosis factor (TNF)-α, IL-6 and IL-8.…”

Section: Introductionmentioning

confidence: 99%

“…6,14 The early responses in endothelial cells involve these cytokines and they take part in re-vascularization, 11,15 and early tissue remodeling after injury 14,16 . IL-6 plays a role in the epithelial repair process 17,18 by regulating the vascular response in airways and by enhancing fibroblast proliferation 11,19 . IL-8, a key mediator in acute inflammation due to its potent attraction of neutrophils 20,21 participates also in the control of endothelial proliferation during angiogenesis.…”

Section: Introductionmentioning

confidence: 99%

IL-1β as a determinant in silica-induced cytokine responses in monocyte-endothelial cell co-cultures

et al. 2008

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Alveolar macrophages and endothelial cells are both involved in lung inflammation and remodeling of lung alveolar structures. In the present study, monocytes (precursors for macrophages) were exposed to crystalline silica and examined for pro- and anti-inflammatory cytokine responses in non-contact co-cultures with endothelial cells. The time courses for silica-induced release of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-8 both from co-cultures and monocyte mono-cultures showed an early peak at 5–10 h, almost no response at 20 h, and a strong increase at 43 h. At 43 h, co-cultures also showed strongly increased IL-6 levels. Steady-state levels of mRNA roughly exhibited the same pattern of early up-regulation and reduced levels at 20 h. Compared with monocyte mono-cultures, silica induced a strong release of IL-1β, IL-6, and IL-8, but not of TNF-α, after 43 h in co-cultures, whereas at 5 and 10 h a significant difference was only observed for the silica-induced IL-8 response. An antagonist to the IL-1 receptor strongly reduced IL-6 and IL-8 levels, whereas antibodies to TNF-α increased the levels of IL-1β and IL-8. Thus, IL-1β is suggested to be an important triggering factor that determines the silica-induced release of several of the other cytokines in this co-culture system.

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Angiogenesis in paediatric airway disease

Cited by 23 publications

References 117 publications

Pathogenesis of Asthma

Pathogenesis of Asthma

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

IL-1β as a determinant in silica-induced cytokine responses in monocyte-endothelial cell co-cultures

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