The Production of Extracellular Matrix Proteins by Human Passively Sensitized Airway Smooth-Muscle Cells in Culture

Johnson, Peter R.; Black, Judith L.; Carlin, Stephen M.; Ge, Qi; Underwood, P.A.

doi:10.1164/ajrccm.162.6.9909111

Cited by 142 publications

(128 citation statements)

References 33 publications

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“…Serum from an asthmatic individual has previously been shown to increase production of laminin c1 chains and other ECM components (i.e. fibronectin, perlecan and chondroitin sulphate) by human airway smooth muscle cells in vitro [45]. However, beclomethasone treatment failed to reduce this stimulatory effect of the asthmatic serum [45].…”

Section: Discussionmentioning

confidence: 99%

“…fibronectin, perlecan and chondroitin sulphate) by human airway smooth muscle cells in vitro [45]. However, beclomethasone treatment failed to reduce this stimulatory effect of the asthmatic serum [45]. In one study of 10 patients with severe asthma, despite longterm corticosteroid treatment (mean 3.7 yrs), the asthmatic subjects showed thickening of basement membrane reticular collagen comparable to controls without asthma [46].…”

Section: Discussionmentioning

confidence: 99%

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Increase in laminin expression in allergic airway remodelling and decrease by dexamethasone

Pe¹,

Jonas²,

Tsai³

et al. 2004

European Respiratory Journal

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Lung expression of the extracellular matrix protein, laminin, and its receptor, laminin-1 receptor, were examined in a mouse model of asthma with airway remodelling.Ovalbumin (OVA) was administered to BALB/c mice, intraperitoneally on days 0 and 14, and intranasally periodically between days 14 and 75.The mice developed airway eosinophil and mononuclear inflammatory cell infiltration and fibrosis. On day 76, a marked increase in total laminin was seen in the airways of OVA-treated mice compared to controls by Western blot analysis. The increased laminin expression was detected immunocytochemically in the thickened subepithelial basement membrane and around airways and blood vessels. The OVA-treated mice showed increased expression of the a1, b1, and c1 chains of the laminin-1 isoform in monocytes, macrophages and eosinophils infiltrating the airways. Laminin-1 receptor expression was increased in inflammatory and endothelial cells in the lungs of OVAtreated mice compared to controls. Treatment of OVA-sensitised/challenged mice with dexamethasone reduced airway expression of laminin and laminin-1 receptor in OVAtreated mice but not airway hyperresponsiveness to methacholine.Laminin deposition may be an important component of the airway remodelling observed in chronic allergic lung inflammation and is a process modulated by corticosteroids.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Increase in laminin expression in allergic airway remodelling and decrease by dexamethasone

Pe¹,

Jonas²,

Tsai³

et al. 2004

European Respiratory Journal

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show abstract

“…Several of these characteristics have been described in both large and small airways [39]. Cultured human nonasthmatic BSM cells produce a wide range of matrix proteins, including fibronectin, perlecan, elastin, laminin, thrombospondin, chondroitin sulfate, collagen I, III, IV and V, versican and decorin [40]. Interestingly, asthmatic BSM cells produce an altered profile of ECM proteins in vitro, characterised by more collagen I and perlecan, but less laminin-a1, collagen IV [41] and hyaluronan [42].…”

Section: Altered Ecm Within the Smooth Muscle Layermentioning

confidence: 99%

Pathophysiology of bronchial smooth muscle remodelling in asthma

Bara¹,

Ozier²,

Lara³

et al. 2010

European Respiratory Journal

148

136

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Whereas the role of bronchial smooth muscle remains controversial in healthy subjects its role is well established in asthmatics. Bronchial smooth muscle contraction induces airway narrowing. The smooth muscle also contributes to bronchial inflammation by secreting a range of inflammatory mediators, recruiting and activating inflammatory cells, such as mast cells or T-lymphocytes. In addition, bronchial smooth muscle mass is significantly increased in asthma. Such an increase has been related to a deposition of extracellular matrix proteins, and an increase in both cell size and number. However, the mechanisms of this smooth muscle remodelling are complex and not completely understood. The article will review recent data regarding the pathophysiology of bronchial smooth muscle remodelling in asthma.

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“…ASM cells are directly involved in this cycle, perpetuating lung inflammation (40). In addition, human ASM cells in culture can also produce several compounds implicated in remodeling, including fibronectin, laminin, percelan, chondroitin, and vascular endothelial growth factor (42,43,45,46). This may be especially relevant in the presence of increased smooth muscle mass observed in asthmatic lungs (35).…”

Section: Airway Inflammationmentioning

confidence: 99%

Asthma: where is it going?

Faffe¹

2008

Braz J Med Biol Res

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Asthma is characterized by reversible airway obstruction, airway hyperresponsiveness, and airway inflammation. Although our understanding of its pathophysiological mechanisms continues to evolve, the relative contributions of airway hyperresponsiveness and inflammation are still debated. The first mechanism identified as important for asthma was bronchial hyperresponsiveness. In a second step, asthma was recognized also as an inflammatory disease, with chronic inflammation inducing structural changes or remodeling. However, persistence of airway dysfunction despite inflammatory control is observed in chronic severe asthma of both adults and children. More recently, a potential role for epithelial-mesenchymal communication or transition is emerging, with epithelial injury often resulting in a self-sustaining phenotype of wound repair modulation by activation/ reactivation of the epithelial-mesenchymal trophic unit, suggesting that chronic asthma can be more than an inflammatory disease. It is noteworthy that the gene-environmental interactions critical for the development of a full asthma phenotype involve processes similar to those occurring in branching morphogenesis. In addition, a central role for airway smooth muscle in the pathogenesis of the disease has been explored, highlighting its secretory function as well as different intrinsic properties compared to normal subjects. These new concepts can potentially shed light on the mechanisms underlying some asthma phenotypes and improve our understanding of the disease in terms of the therapeutic strategies to be applied. How we understand asthma and its mechanisms along time will be the focus of this overview.

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The Production of Extracellular Matrix Proteins by Human Passively Sensitized Airway Smooth-Muscle Cells in Culture

Cited by 142 publications

References 33 publications

Increase in laminin expression in allergic airway remodelling and decrease by dexamethasone

Increase in laminin expression in allergic airway remodelling and decrease by dexamethasone

Pathophysiology of bronchial smooth muscle remodelling in asthma

Asthma: where is it going?

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