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Molecular Pharmacology

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Research ArticleArticle

Interleukin 13 Increases Contractility of Murine Tracheal Smooth Muscle by a Phosphoinositide 3-kinase p110δ-Dependent Mechanism

Hanan S. M. Farghaly, Ian S. Blagbrough, David A. Medina-Tato and Malcolm L. Watson
Molecular Pharmacology May 2008, 73 (5) 1530-1537; DOI: https://doi.org/10.1124/mol.108.045419
Hanan S. M. Farghaly
Department of Pharmacy and Pharmacology, University of Bath, Bath, United Kingdom
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Ian S. Blagbrough
Department of Pharmacy and Pharmacology, University of Bath, Bath, United Kingdom
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David A. Medina-Tato
Department of Pharmacy and Pharmacology, University of Bath, Bath, United Kingdom
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Malcolm L. Watson
Department of Pharmacy and Pharmacology, University of Bath, Bath, United Kingdom
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Abstract

The Th2 cytokine interleukin (IL) 13 can elicit a number of responses consistent with a key role in the pathogenesis of asthma. We have used pharmacological and genetic approaches to demonstrate the role of signaling via the class I phosphoinositide 3-kinase p110δ isoform in IL-13-induced hyper-responsiveness of murine tracheal smooth muscle contractility in vitro. IL-13 treatment of tracheal tissue is associated with an early activation of phosphoinositide 3-kinase (PI3K), as assessed by phosphorylation of Akt. Tracheal smooth muscle contractility is enhanced by overnight incubation with IL-13, resulting in increased maximal contractions (Emax) to carbachol (CCh) and KCl. Inhibition of PI3K by the non-isoform-selective inhibitors wortmannin or 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one (LY294002), or the selective inhibitor of the PI3K p110δ isoform 2-(6-aminopurin-9-ylmethyl)-5-methyl-3-O-tolyl-3H-quinazolin-4-one (IC87114), prevented IL-13-induced hyper-responsiveness. Consistent with a role for PI3K p110δ in IL-13-induced hyper-responsiveness, IL-13 was unable to induce hyper-responsiveness in tissues from mice expressing the catalytically inactive form of p110δ (p110δD910A). These data indicate that IL-13 contributes to tracheal smooth muscle hyper-responsiveness via the PI3K p110δ isoform. In addition to previously reported effects on airway inflammation, inhibition of PI3K p110δ may be a useful target for the treatment of asthma by preventing IL-13-induced airway smooth muscle hyper-responsiveness.

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Molecular Pharmacology: 73 (5)
Molecular Pharmacology
Vol. 73, Issue 5
1 May 2008
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Research ArticleArticle

Interleukin 13 Increases Contractility of Murine Tracheal Smooth Muscle by a Phosphoinositide 3-kinase p110δ-Dependent Mechanism

Hanan S. M. Farghaly, Ian S. Blagbrough, David A. Medina-Tato and Malcolm L. Watson
Molecular Pharmacology May 1, 2008, 73 (5) 1530-1537; DOI: https://doi.org/10.1124/mol.108.045419

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Research ArticleArticle

Interleukin 13 Increases Contractility of Murine Tracheal Smooth Muscle by a Phosphoinositide 3-kinase p110δ-Dependent Mechanism

Hanan S. M. Farghaly, Ian S. Blagbrough, David A. Medina-Tato and Malcolm L. Watson
Molecular Pharmacology May 1, 2008, 73 (5) 1530-1537; DOI: https://doi.org/10.1124/mol.108.045419
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