Remodeling in asthma

Al‐Muhsen, Saleh; Johnson, Jill; Hamid, Qutayba

doi:10.1016/j.jaci.2011.04.047

Cited by 371 publications

(322 citation statements)

References 200 publications

(204 reference statements)

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“…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%

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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Section: Tissue Remodeling and Angiogenesismentioning

confidence: 99%

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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“…An increase in BSMC mass and decreased distance between BSMC and epithelium are hallmark features of the remodeled wall in asthmatic airways (2). These changes in BSMCs may be induced by factors produced by epithelium (30).…”

Section: The CM Of Both Ykl-40-treated Beas-2b Cells and Ykl-40-treatmentioning

confidence: 99%

“…It is now believed that chronic inflammation drives the remodeling response, leading to structural alterations responsible for pathogenesis and clinical manifestations of asthma (2). Among these alterations, increased bronchial smooth muscle cell (BSMC) mass may represent a key feature contributing to airflow obstruction (3).…”

mentioning

confidence: 99%

YKL-40 Induces IL-8 Expression from Bronchial Epithelium via MAPK (JNK and ERK) and NF-κB Pathways, Causing Bronchial Smooth Muscle Proliferation and Migration

Tang

Sun

Shi

et al. 2013

The Journal of Immunology

108

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Recently, the serum levels of YKL-40, a chitinase-like glycoprotein, have been shown to be significantly elevated in asthmatics and are associated with asthma severity. Although these studies raise the possibility that YKL-40 may influence asthma, the mechanisms remain unknown. This study firstly investigated the mechanisms involved in YKL-40–mediated inflammation in human bronchial epithelial cells (HBECs) and analyzed the soluble factors secreted by bronchial epithelial cells exposed to YKL-40 that were responsible for increasing proliferation and migration of primary normal human bronchial smooth muscle cells (BSMCs). YKL-40–induced inflammation was assayed in two HBECs (BEAS-2B cell line and primary HBECs). In addition, we treated BEAS-2B cells and HBECs with YKL-40 and added the conditioned culture media to BSMCs. The proliferation and migration of BSMCs were determined by premixed WST-1 cell proliferation reagent (Clontech Laboratories) and QCM chemotaxis migration assay (Millipore), respectively. Bronchial epithelial cells treated with YKL-40 resulted in a significant increase of IL-8 production, which was dependent on MAPK (JNK and ERK) and NF-κB pathways activation. YKL-40–induced IL-8 was found to further stimulate proliferation and migration of BSMCs, and the effects were inhibited after neutralizing IL-8. Through investigating the interaction of airway epithelium and smooth muscle, our findings implicate that YKL-40 may be involved in the inflammation of asthma by induction of IL-8 from epithelium, subsequently contributing to BSMC proliferation and migration. Moreover, inhibition of IL-8 signaling is a potential therapeutic target for YKL-40–induced inflammation and remodeling of asthma.

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“…Tissue remodelling due to increased BSM mass in allergic asthma is also known to correlate with airway hyper-responsiveness and severity of asthma in patients. Taken together, smooth muscle amount, and changes in its mass are likely to be key players in the dynamics of airway narrowing, including increased airway hyper-responsiveness and basic bronchial tension (6,8). However, according to the morphometric analysis of structure changes -collagen deposition, α-smooth muscle actin expression -impaired bronchoprotection induced by chronic FORM treatment seems to have no relevance with increased smooth muscle mass.…”

Section: Discussionmentioning

confidence: 99%

“…Smooth muscle (SM) α-actin is the first smooth muscle cell differentiation marker to appear during development and is also expressed in fibroblast differentiation to smooth muscle cell during airway remodelling or repairing; moreover, its expression is primarily restricted to smooth muscle cell in adult animals. Therefore, α-actin is the ideal marker of smooth muscle cells (8).…”

Section: Introductionmentioning

confidence: 99%

Impaired Bronchoprotection Is Not Induced by Increased Smooth Muscle Mass in Chronic Treatment In Vivo with Formoterol in Asthmatic Mouse Model

Luo¹,

Ct²,

Qin³

et al. 2014

WIMJ Open

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Remodeling in asthma

Cited by 371 publications

References 200 publications

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

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

YKL-40 Induces IL-8 Expression from Bronchial Epithelium via MAPK (JNK and ERK) and NF-κB Pathways, Causing Bronchial Smooth Muscle Proliferation and Migration

Impaired Bronchoprotection Is Not Induced by Increased Smooth Muscle Mass in Chronic Treatment In Vivo with Formoterol in Asthmatic Mouse Model

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