Gene expression of vascular endothelial growth factor and its receptors and angiogenesis in bronchial asthma

Hoshino, Makoto; Nakamura, Yutaka; Hamid, Qutayba

doi:10.1067/mai.2001.115626

Cited by 255 publications

(208 citation statements)

References 27 publications

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“…Interestingly, VEGF production by airway structural cells are induced by T H 17 cells [52] and suppressed by T H 1 cells [53]. Increased protein levels of VEGF are observed in bronchoalveolar lavage fluid (BALf), sputum and bronchial biopsies of asthma and COPD patients [11,13,48,54]. VEGF is constitutively synthesised by ASM cells in vitro, whereas this production can be altered in response to a number of stimuli, such as TNF-α, TGF-β1, IL-1β, angiotensin II, endothelin-1 and nitric oxide [28,55,56].…”

Section: Angiogenesis and Vascular Endothelial Growth Factormentioning

confidence: 99%

Pulmonary vascular changes in asthma and COPD

Harkness

Kanabar

Sharma

et al. 2014

Pulmonary Pharmacology & Therapeutics

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In chronic lung disorders such as in asthma and chronic obstructive pulmonary disease (COPD) there is increased bronchial angiogenesis and remodelling of pulmonary vessels culminating to altered bronchial and pulmonary circulation. The involvement of residential cells such as endothelial cells, smooth muscle cells and pulmonary fibroblasts, all appear to have a crucial role in the progression of vascular inflammation and remodelling. The regulatory abnormalities, growth factors and mediators implicated in the pulmonary vascular changes of asthma and COPD subjects and potential therapeutic targets have been described in this review.

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Section: Angiogenesis and Vascular Endothelial Growth Factormentioning

confidence: 99%

Pulmonary vascular changes in asthma and COPD

Harkness

Kanabar

Sharma

et al. 2014

Pulmonary Pharmacology & Therapeutics

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“…Angiogenesis is also a feature of airway remodelling in asthmatic individuals. The formation of new vessels within the lung parenchyma is inversely correlated to airway calibre and airways hyperresponsiveness (Hoshino et al, 2001).…”

Section: Platelets and Tissue Remodelling Eventsmentioning

confidence: 99%

Novel uses for anti‐platelet agents as anti‐inflammatory drugs

Pitchford

2007

British J Pharmacology

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An alteration in the character and function of platelets is manifested in patients with inflammatory diseases, and these alterations have been dissociated from the well‐characterized involvement of platelets in thrombosis and haemostasis. Recent evidence reveals platelet activation is sometimes critical in the development of inflammation. The mechanisms by which platelets participate in inflammation are diverse, and offer numerous opportunities for future drug intervention. There is now acceptance that platelets act as innate inflammatory cells in immune responses, with roles as sentinel cells undergoing surveillance, responding to microbial invasion, orchestrating leukocyte recruitment, and migrating through tissue, causing damage and influencing repair processes in chronic disease. Some of these processes are targeted by drugs that are being developed to target platelet participation in atherosclerosis. The actions of platelets therefore influence the pathogenesis of diverse inflammatory diseases in various body compartments, encompassing parasitic and bacterial infection, allergic inflammation (especially asthma and rhinitis), and non‐atopic inflammatory conditions, for example, chronic obstructive pulmonary disease (COPD), rheumatoid arthritis (RA), inflammatory bowel disease (IBD) and atherosclerosis. This review will first discuss the evidence for platelet activation in these various inflammatory diseases, and secondly discuss the mechanisms by which this pathogenesis occurs and the various anti‐platelet agents which have been developed to combat platelet activation in atherosclerosis and their potential future use for the treatment of other inflammatory diseases.British Journal of Pharmacology (2007) 152, 987–1002; doi:10.1038/sj.bjp.0707364; published online 2 July 2007

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“…Our results also indicate that plasma extravasation caused by increased vascular permeability is elevated after inducing asthma and that administration of OTC significantly reduces the increased plasma extravasation. VEGF plays a critical role in asthma (Hoshino et al, 2001;Lee and Lee, 2001;Lee et al, 2004a). One of the major roles of VEGF in asthma appears to be the enhancement of vascular permeability.…”

Section: Discussionmentioning

confidence: 99%

“…The mechanism of VEGF-mediated induction of the vascular permeability seems to be the enhanced functional activity of vesicular-vacuolar organelles (Dvorak et al, 1995). VEGF can be produced by a wide variety of cells including macrophages, neutrophils, eosinophils, and lymphocytes (Horiuchi and Weller, 1997;Taichman et al, 1997;Hoshino et al, 2001;Lee et al, 2002;Lee et al, 2004a;Lee et al, 2004b). Several studies have shown that overproduction of VEGF causes an increase in vascular permeability, which results in leakage of plasma proteins, including inflammatory mediators and cells, into the extravascular space and allowing the migration of inflammatory cells into the airways (Thurston et al, 2000;Lee et al, 2002;Lee et al, 2004b).…”

Section: Discussionmentioning

confidence: 99%

An antioxidant modulates expression of receptor activator of NF-κB in asthma

Lee

Park²,

Park³

et al. 2006

Exp Mol Med

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Oxidative stress plays critical roles in airway inflammation that is usually accompanied by increased vascular permeability and plasma exudation. VEGF increases vascular permeability and leads to airway inflammation. In addition, VEGF has been shown to enhance receptor activator of NF-κB (RANK) expression in endothelial cells. An aim of the study was to determine the potential role of antioxidant in the regulation of RANK expression in murine model of asthma. We have used a C57BL/6 mouse model of allergic asthma to evaluate the effect of L-2-oxothiazolidine-4-carboxylic acid (OTC), a prodrug of cysteine, which acts as an antioxidant, and VEGF receptor inhibitor on RANK mRNA expression. The mice develop the following pathophysiological features of asthma in the lungs: increased expression of RANK mRNA, increased number of inflammatory cells of the airways, increased vascular permeability, and increased levels of VEGF. Administration of OTC and VEGF receptor inhibitor markedly reduced plasma extravasation and VEGF levels in allergen-induced asthmatic lungs. We also showed that the increased RANK mRNA expression at 72 h after ovalbumin inhalation were reduced by the administration of OTC or VEGF receptor inhibitor. The results indicate that OTC and VEGF receptor inhibitor which inhibit up-regulation of VEGF expression modulate RANK expression that may be in association with the regulation of vascular permeability, and suggest that VEGF may regulate the RANK expression. These findings provide a crucial molecular mechanism for the potential use of antioxidants to prevent and/or treat asthma and other airway inflammatory disorders.

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Gene expression of vascular endothelial growth factor and its receptors and angiogenesis in bronchial asthma

Cited by 255 publications

References 27 publications

Pulmonary vascular changes in asthma and COPD

Pulmonary vascular changes in asthma and COPD

Novel uses for anti‐platelet agents as anti‐inflammatory drugs

An antioxidant modulates expression of receptor activator of NF-κB in asthma

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