Cyclic AMP-Mobilizing Agents and Glucocorticoids Modulate Human Smooth Muscle Cell Migration

Goncharova, Elena A.; Billington, Charlotte K.; Irani, Carla; Vorotnikov, Alexander V.; Tkachuk, Vsevolod A.; Penn, Raymond B.; Krymskaya, Vera P.; Panettieri, Reynold A.

doi:10.1165/rcmb.2002-0254oc

Cited by 105 publications

(97 citation statements)

References 56 publications

(69 reference statements)

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“…Compared with salmeterol or dexamethasone alone, the combination of the two agents synergistically inhibited migration of human airway smooth muscle cells induced by platelet-derived growth factor (105). Similarly, the combination of formoterol and budesonide synergistically inhibited serum-induced proliferation and induced enhanced activation of p21 WAF1/Cip1 stimulated with fetal bovine serum in airway smooth muscle cells (106).…”

Section: Airway Smooth Muscle and Effects Of Therapymentioning

confidence: 99%

The Role of Airway Smooth Muscle in the Pathogenesis of Airway Wall Remodeling in Chronic Obstructive Pulmonary Disease

Chung¹

2005

Proceedings of the American Thoracic Society

103

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Airway wall remodeling processes are present in the small airways of patients with chronic obstructive pulmonary disease, consisting of tissue repair and epithelial metaplasia that contribute to airway wall thickening and airflow obstruction. With increasing disease severity, there is also increased mucous metaplasia and submucosal gland hypertrophy, peribronchial fibrosis, and an increase in airway smooth muscle mass. Apart from its contractile properties, airway smooth muscle produces inflammatory cytokines, proteases, and growth factors, which may contribute to the remodeling process and induce phenotypic changes of the muscle. Airflow limitation responds minimally to ␤-agonists and corticosteroid therapy, unlike asthma, perhaps because of alterations in ␤-receptor or glucocorticoid receptor numbers, alterations in receptor signaling, or the constrictive limitation imposed by peribronchial fibrosis. Better response is observed with the combination of inhaled long-acting ␤-agonists and corticosteroids. This could result from effects at the level of airway smooth muscle. Airway wall remodeling may involve the release of growth factors from inflammatory or resident cells. The influence of smoking cessation or of current therapies on airway wall remodeling is unknown. Specific therapies for airway wall remodeling may be necessary, together with noninvasive methods of imaging small airway wall remodeling to assess responses.

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Section: Airway Smooth Muscle and Effects Of Therapymentioning

confidence: 99%

The Role of Airway Smooth Muscle in the Pathogenesis of Airway Wall Remodeling in Chronic Obstructive Pulmonary Disease

Chung¹

2005

Proceedings of the American Thoracic Society

103

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“…Migration is required for each of these alternative mechanisms for smooth muscle hyperplasia. Migration of ASM can be induced by plateletderived growth factor [116,117], enhanced by cys-leukotrienes [118] modulated by b 2 -adrenoceptor agonists and glucocorticoids [119], with the latter agents losing activity when cells are seeded onto a matrix containing monomeric type-1 collagen [120,121].…”

Section: Asm Growth Responsesmentioning

confidence: 99%

Airway smooth muscle dynamics: a common pathway of airway obstruction in asthma

An¹,

Bai²,

Bates³

et al. 2007

European Respiratory Journal

341

298

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Excessive airway obstruction is the cause of symptoms and abnormal lung function in asthma.As airway smooth muscle (ASM) is the effecter controlling airway calibre, it is suspected that dysfunction of ASM contributes to the pathophysiology of asthma. However, the precise role of ASM in the series of events leading to asthmatic symptoms is not clear. It is not certain whether, in asthma, there is a change in the intrinsic properties of ASM, a change in the structure and mechanical properties of the noncontractile components of the airway wall, or a change in the interdependence of the airway wall with the surrounding lung parenchyma. All these potential changes could result from acute or chronic airway inflammation and associated tissue repair and remodelling.Anti-inflammatory therapy, however, does not ''cure'' asthma, and airway hyperresponsiveness can persist in asthmatics, even in the absence of airway inflammation. This is perhaps because the therapy does not directly address a fundamental abnormality of asthma, that of exaggerated airway narrowing due to excessive shortening of ASM.In the present study, a central role for airway smooth muscle in the pathogenesis of airway hyperresponsiveness in asthma is explored.

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“…Airway smooth muscle cells migrate in response to a number of physiologic stimuli in vitro, including PDGF, basic fibroblast growth factor, TGF-b, and IL-1b (93,94). Recent studies suggest that chemokines, small (8-12 kD) proteins involved in the regulation of leukocyte trafficking, may also regulate airway smooth muscle migration.…”

Section: Airway Smooth Muscle Migrationmentioning

confidence: 99%

“…Airway smooth muscle cells also express CXCR1, CXCR2, and CCR7, and migrate in response to the CXCR1/2 ligand IL-8 and the CCR7 ligand CCL19 (96,97). Moreover, b-agonists and corticosteroids inhibit migration (94).…”

Section: Airway Smooth Muscle Migrationmentioning

confidence: 99%

Airway Smooth Muscle Growth in Asthma: Proliferation, Hypertrophy, and Migration

Bentley

Hershenson

2008

Proceedings of the American Thoracic Society

157

128

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Increased airway smooth muscle mass is present in fatal and nonfatal asthma. However, little information is available regarding the cellular mechanism (i.e., hyperplasia vs. hypertrophy). Even less information exists regarding the functional consequences of airway smooth muscle remodeling. It would appear that increased airway smooth muscle mass would tend to increase airway narrowing and airflow obstruction. However, the precise effects of increased airway smooth muscle mass on airway narrowing are not known. This review will consider the evidence for airway smooth muscle cell proliferation and hypertrophy in asthma, potential functional effects, and biochemical mechanisms.

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Cyclic AMP-Mobilizing Agents and Glucocorticoids Modulate Human Smooth Muscle Cell Migration

Cited by 105 publications

References 56 publications

The Role of Airway Smooth Muscle in the Pathogenesis of Airway Wall Remodeling in Chronic Obstructive Pulmonary Disease

The Role of Airway Smooth Muscle in the Pathogenesis of Airway Wall Remodeling in Chronic Obstructive Pulmonary Disease

Airway smooth muscle dynamics: a common pathway of airway obstruction in asthma

Airway Smooth Muscle Growth in Asthma: Proliferation, Hypertrophy, and Migration

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