Angiogenesis in bronchial asthma

Pałgan, Krzysztof; Bartuzi, Zbigniew

doi:10.1177/0394632015580907

Cited by 24 publications

(19 citation statements)

References 29 publications

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“…Inhibition of ERG in human umbilical vein endothelial cells causes loss of cell–cell contact and attenuation of microvessel formation . Angiogenin also appears to play a fundamental, if ill‐defined, role in vascular growth . Amphiregulin is a potent mitogen for several types of cell, including epithelial cells, vascular smooth muscle cells and endothelial cells acting via the EGF receptor .…”

Section: Discussionmentioning

confidence: 99%

Nasal administration of interleukin‐33 induces airways angiogenesis and expression of multiple angiogenic factors in a murine asthma surrogate

Shan

Wang

et al. 2016

Immunology

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SummaryThe T-helper cell type 2-promoting cytokine interleukin-33 (IL-33) has been implicated in asthma pathogenesis. Angiogenesis is a feature of airways remodelling in asthma. We hypothesized that IL-33 induces airways angiogenesis and expression of angiogenic factors in an established murine surrogate of asthma. In the present study, BALB/c mice were subjected to serial intranasal challenge with IL-33 alone for up to 70 days. In parallel, ovalbumin (OVA) -sensitized mice were subjected to serial intranasal challenge with OVA or normal saline to serve as positive and negative controls, respectively. Immunohistochemical analysis of expression of von Willebrand factor and erythroblast transformation-specific-related gene, both blood vessel markers, and angiogenic factors angiogenin, insulin-like growth factor-1, endothelin-1, epidermal growth factor and amphiregulin was performed in lung sections ex vivo. An established inhouse assay was used to test whether IL-33 was able to induce microvessel formation by human vascular endothelial cells. Results showed that serial intranasal challenge of mice with IL-33 or OVA resulted in proliferation of peribronchial von Willebrand factor-positive blood vessels to a degree closely related to the total expression of the angiogenic factors amphiregulin, angiogenin, endothelin-1, epidermal growth factor and insulin-like growth factor-1. IL-33 also induced microvessel formation by human endothelial cells in a concentration-dependent fashion in vitro. Our data are consistent with the hypothesis that IL-33 has the capacity to induce angiogenesis at least partly by increasing local expression of multiple angiogenic factors in an allergen-independent murine asthma surrogate, and consequently that IL-33 or its receptor is a potential novel molecular target for asthma therapy.

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Section: Discussionmentioning

confidence: 99%

Nasal administration of interleukin‐33 induces airways angiogenesis and expression of multiple angiogenic factors in a murine asthma surrogate

Shan

Wang

et al. 2016

Immunology

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“…Asthma is characterized by reversible airflow obstruction that is initiated by chronic and oftentimes allergic bronchial wall inflammation and bronchial wall remodeling (Pałgan and Bartuzi 2015). CS and air pollution were found to enhance the risk for developing asthma (Ferrante et al 2014) and are thought to trigger acute exacerbations in patients with established asthma (Guarnieri and Balmes 2014;Wang et al 2015).…”

Section: Asthma and Occupational Asthmamentioning

confidence: 99%

“…Epithelial-to-mesenchymal transition and remodeling of the extracellular matrix are important processes in COPD and lung cancer development (Houghton 2013). Thickening of the bronchial subepithelial layer and fibroblast-to-myofibroblast differentiation are also involved in COPD and asthma pathogenesis (Al-Muhsen, Johnson, and Hamid 2011;Pałgan and Bartuzi 2015;Salazar and Herrera 2011). Finally, extracellular matrix degradation may contribute to (1) emphysema formation (Salazar and Herrera 2011) and (2) destabilization of atherosclerotic plaques, enhancing risk for cardiovascular complications (Messner and Bernhard 2014).…”

Section: Tissue Remodeling and Angiogenesismentioning

confidence: 99%

“…In atherosclerosis, the formation of leaky intraplaque neovessels contributes to plaque destabilization (Michel et al 2014). Finally, in asthma, subepithelial angiogenesis promotes thickening of the subepithelial layer and facilitates infiltration of immune cells into the bronchial wall (Pałgan and Bartuzi 2015). Eleven studies were identified that investigated whether EV secreted in response to respiratory exposures promote tissue degradation, remodeling, or angiogenesis.…”

Section: Tissue Remodeling and Angiogenesismentioning

confidence: 99%

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Extracellular vesicles released in response to respiratory exposures: implications for chronic disease

Benedikter

Wouters

Savelkoul

et al. 2018

Journal of Toxicology and Environmental Health, Part B

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Extracellular vesicles (EV) are secreted signaling entities that enhance various pathological processes when released in response to cellular stresses. Respiratory exposures such as cigarette smoke and air pollution exert cellular stresses and are associated with an increased risk of several chronic diseases. The aim of this review was to examine the evidence that modifications in EV contribute to respiratory exposure-associated diseases. Publications were searched using PubMed and Google Scholar with the search terms (cigarette smoke OR tobacco smoke OR air pollution OR particulate matter) AND (extracellular vesicles OR exosomes OR microvesicles OR microparticles OR ectosomes). All original research articles were included and reviewed. Fifty articles were identified, most of which investigated the effect of respiratory exposures on EV release in vitro (25) and/or on circulating EV in human plasma (24). The majority of studies based their main observations on the relatively insensitive scatter-based flow cytometry of EV (29). EV induced by respiratory exposures were found to modulate inflammation (19), thrombosis (13), endothelial dysfunction (11), tissue remodeling (6), and angiogenesis (3). By influencing these processes, EV may play a key role in the development of cardiovascular diseases and chronic obstructive pulmonary disease and possibly lung cancer and allergic asthma. The current findings warrant additional research with improved methodologies to evaluate the contribution of respiratory exposure-induced EV to disease etiology, as well as their potential as biomarkers of exposure or risk and as novel targets for preventive or therapeutic strategies.

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“…Asthma is characterized by reversible airflow obstruction that is initiated by chronic and oftentimes allergic bronchial wall inflammation and bronchial wall remodeling (Palgan and Bartuzi 2015). CS and air pollution were found to enhance the risk for developing asthma (Ferrante et al 2014) and are thought to trigger acute exacerbations in patients with established asthma (Guarnieri and…”

Section: Asthma and Occupational Asthmamentioning

confidence: 99%

Extracellular vesicles as mediators of the response to respiratory exposures

Benedikter¹

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Angiogenesis in bronchial asthma

Cited by 24 publications

References 29 publications

Nasal administration of interleukin‐33 induces airways angiogenesis and expression of multiple angiogenic factors in a murine asthma surrogate

Nasal administration of interleukin‐33 induces airways angiogenesis and expression of multiple angiogenic factors in a murine asthma surrogate

Extracellular vesicles released in response to respiratory exposures: implications for chronic disease

Extracellular vesicles as mediators of the response to respiratory exposures

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