Literature DB >> 16159613

Airway smooth muscle: a modulator of airway remodeling in asthma.

Aili L Lazaar1, Reynold A Panettieri.   

Abstract

Asthma is a disease characterized, in part, by airway hyperresponsiveness and inflammation. Although asthma typically induces reversible airway obstruction, in some patients with asthma, airflow obstruction can become irreversible. Such obstruction might be a consequence of persistent structural changes in the airway wall caused by the frequent stimulation of airway smooth muscle (ASM) by contractile agonists, inflammatory mediators, and growth factors. Traditional concepts concerning airway inflammation have focused on trafficking leukocytes and on the effects of inflammatory mediators, cytokines, and chemokines secreted by these cells. Recent studies suggest that ASM cells might modulate airway remodeling by secreting cytokines, growth factors, or matrix proteins and by expressing cell adhesion molecules and other potential costimulatory molecules. These ASM cell functions might directly or indirectly modulate submucosal airway inflammation and promote airway remodeling.

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Year:  2005        PMID: 16159613     DOI: 10.1016/j.jaci.2005.06.030

Source DB:  PubMed          Journal:  J Allergy Clin Immunol        ISSN: 0091-6749            Impact factor:   10.793


  52 in total

1.  Oxidant signaling for interleukin-13 gene expression in lung smooth muscle cells.

Authors:  Geetanjali Bansal; Chi-Ming Wong; Lingling Liu; Yuichiro J Suzuki
Journal:  Free Radic Biol Med       Date:  2012-02-25       Impact factor: 7.376

Review 2.  Does airway smooth muscle express an inflammatory phenotype in asthma?

Authors:  Gautam Damera; Reynold A Panettieri
Journal:  Br J Pharmacol       Date:  2011-05       Impact factor: 8.739

3.  The extract of Cordyceps sinensis inhibited airway inflammation by blocking NF-κB activity.

Authors:  Ya-Ling Chiou; Ching-Yuang Lin
Journal:  Inflammation       Date:  2012-06       Impact factor: 4.092

4.  Airway smooth muscle relaxation is impaired in mice lacking the p47phox subunit of NAD(P)H oxidase.

Authors:  Pasquale Chitano; Lu Wang; Stanley N Mason; Richard L Auten; Erin N Potts; William M Foster; Anne Sturrock; Thomas P Kennedy; John R Hoidal; Thomas M Murphy
Journal:  Am J Physiol Lung Cell Mol Physiol       Date:  2007-11-09       Impact factor: 5.464

5.  Nuclear translocation of p65 NF-kappaB is sufficient for VCAM-1, but not ICAM-1, expression in TNF-stimulated smooth muscle cells: Differential requirement for PARP-1 expression and interaction.

Authors:  Mourad Zerfaoui; Yasuhiro Suzuki; Amarjit S Naura; Chetan P Hans; Charles Nichols; A Hamid Boulares
Journal:  Cell Signal       Date:  2007-10-12       Impact factor: 4.315

6.  Do biophysical properties of the airway smooth muscle in culture predict airway hyperresponsiveness?

Authors:  Steven S An; Ben Fabry; Xavier Trepat; Ning Wang; Jeffrey J Fredberg
Journal:  Am J Respir Cell Mol Biol       Date:  2006-02-16       Impact factor: 6.914

Review 7.  Embracing emerging paradigms of G protein-coupled receptor agonism and signaling to address airway smooth muscle pathobiology in asthma.

Authors:  Raymond B Penn
Journal:  Naunyn Schmiedebergs Arch Pharmacol       Date:  2008-02-16       Impact factor: 3.000

8.  Airway smooth muscle in bronchial tone, inflammation, and remodeling: basic knowledge to clinical relevance.

Authors:  Reynold A Panettieri; Michael I Kotlikoff; William T Gerthoffer; Marc B Hershenson; Prescott G Woodruff; Ian P Hall; Susan Banks-Schlegel
Journal:  Am J Respir Crit Care Med       Date:  2007-11-15       Impact factor: 21.405

Review 9.  Mechanistic systems biology of inflammatory gene expression in airway smooth muscle as tool for asthma drug development.

Authors:  Chi-Ming Hai
Journal:  Curr Drug Discov Technol       Date:  2008-12

Review 10.  Biophysical basis for airway hyperresponsiveness.

Authors:  Steven S An; Jeffrey J Fredberg
Journal:  Can J Physiol Pharmacol       Date:  2007-07       Impact factor: 2.273

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