ArticleThe Journal of pharmacology and experimental therapeutics2012
Targeting phosphoinositide 3-kinase γ in airway smooth muscle cells to suppress interleukin-13-induced mouse airway hyperresponsiveness.
Article in The Journal of pharmacology and experimental therapeutics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- Degradation of IL-4Ralpha by Immunoproteasome: implication in airway type 2 inflammation and hyperresponsiveness.Frontiers in immunology · 2025Article
- Role of GLCCI1 in inhibiting PI3K-induced NLRP3 inflammasome activation in asthma.Chinese medical journal pulmonary and critical care medicine · 2024Article
- Precision cut lung slices: an integrated ex vivo model for studying lung physiology, pharmacology, disease pathogenesis and drug discovery.Respiratory research · 2024Review
- Identifying Active Compounds and Mechanisms ofEvidence-based complementary and alternative medicine : eCAM · 2022Article
- Different effects of acetyl-CoA carboxylase inhibitor TOFA on airway inflammation and airway resistance in a mice model of asthma.Pharmacological reports : PR · 2020Article
- Preserving Airway Smooth Muscle Contraction in Precision-Cut Lung Slices.Scientific reports · 2020Article
- Detecting the Multiomics Signatures of Factor-Specific Inflammatory Effects on Airway Smooth Muscles.Frontiers in genetics · 2020Article
- Use of precision cut lung slices as a translational model for the study of lung biology.Respiratory research · 2019Review
- Hypercapnia increases airway smooth muscle contractility via caspase-7-mediated miR-133a-RhoA signaling.Science translational medicine · 2018Article
- Overexpression of miR-155-5p Inhibits the Proliferation and Migration of IL-13-Induced Human Bronchial Smooth Muscle Cells by Suppressing TGF-β-Activated Kinase 1/MAP3K7-Binding Protein 2.Allergy, asthma & immunology research · 2018Article
- Inhibition of PI3K promotes dilation of human small airways in a rho kinase-dependent manner.British journal of pharmacology · 2016Article
- Early-Life Intranasal Colonization with Nontypeable Haemophilus influenzae Exacerbates Juvenile Airway Disease in Mice.Infection and immunity · 2016Article
- Regulator of G-protein signaling 2 repression exacerbates airway hyper-responsiveness and remodeling in asthma.American journal of respiratory cell and molecular biology · 2015Article
- AS252424, a PI3Kγ inhibitor, downregulates inflammatory responsiveness in mouse bone marrow-derived mast cells.Inflammation · 2014Article
- Identification of upregulated phosphoinositide 3-kinase γ as a target to suppress breast cancer cell migration and invasion.Biochemical pharmacology · 2013Article
- Fish oil has beneficial effects on allergen-induced airway inflammation and hyperreactivity in mice.PloS one · 2013Article
- Dietary acacetin reduces airway hyperresponsiveness and eosinophil infiltration by modulating eotaxin-1 and th2 cytokines in a mouse model of asthma.Evidence-based complementary and alternative medicine : eCAM · 2012Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
We recently reported that phosphoinositide 3-kinase γ (PI3Kγ) directly regulates airway smooth muscle (ASM) contraction by modulating Ca(2+) oscillations. Because ASM contraction plays a critical role in airway hyperresponsiveness (AHR) of asthma, the aim of the present study was to determine whether targeting PI3Kγ in ASM cells could suppress AHR in vitro and in vivo. Intranasal administration into mice of interleukin-13 (IL-13; 10 μg per mouse), a key pathophysiologic cytokine in asthma, induced AHR after 48 h, as assessed by invasive tracheostomy. Intranasal administration of a broad-spectrum PI3K inhibitor or a PI3Kγ-specific inhibitor 1 h before AHR assessment attenuated IL-13 effects. Airway responsiveness to bronchoconstrictor agonists was also examined in precision-cut mouse lung slices pretreated without or with IL-13 for 24 h. Acetylcholine and serotonin dose-response curves indicated that IL-13-treated lung slices had a 40 to 50% larger maximal airway constriction compared with controls. Furthermore, acetylcholine induced a larger initial Ca(2+) transient and increased Ca(2+) oscillations in IL-13-treated primary mouse ASM cells compared with control cells, correlating with increased cell contraction. As expected, PI3Kγ inhibitor treatment attenuated IL-13-augmented airway contractility of lung slices and ASM cell contraction. In both control and IL-13-treated ASM cells, small interfering RNA-mediated knockdown of PI3Kγ by 70% only reduced the initial Ca(2+) transient by 20 to 30% but markedly attenuated Ca(2+) oscillations and contractility of ASM cells by 50 to 60%. This report is the first to demonstrate that PI3Kγ in ASM cells is important for IL-13-induced AHR and that acute treatment with a PI3Kγ inhibitor can ameliorate AHR in a murine model of asthma.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.