ArticleThe Journal of allergy and clinical immunology2014
Loss of regulator of G protein signaling 5 promotes airway hyperresponsiveness in the absence of allergic inflammation.
Article in The Journal of allergy and clinical immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 37 citations in OpenAlex.
- Sema3E-plexinD1 Axis Is a Modulator of Foxp3FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Beyond the Usual Suspects: Unmasking Low-T2 Asthma in Children.Journal of clinical medicine · 2026Review
- Precision cut lung slices: an integrated ex vivo model for studying lung physiology, pharmacology, disease pathogenesis and drug discovery.Respiratory research · 2024Review
- Gut-lung axis and asthma: A historical review on mechanism and future perspective.Clinical and translational allergy · 2024Review
- RGS4 controls airway hyperresponsiveness through GAP-independent mechanisms.The Journal of biological chemistry · 2024Article
- The potential role of n-3 fatty acids and their lipid mediators on asthmatic airway inflammation.Frontiers in immunology · 2024Review
- Resmetirom Ameliorates NASH-Model Mice by Suppressing STAT3 and NF-κB Signaling Pathways in an RGS5-Dependent Manner.International journal of molecular sciences · 2023Article
- Targeted Inhibition of Select Extracellular Signal-regulated Kinases 1 and 2 Functions Mitigates Pathological Features of Asthma in Mice.American journal of respiratory cell and molecular biology · 2023Article
- Paucigranulocytic Asthma: Potential Pathogenetic Mechanisms, Clinical Features and Therapeutic Management.Journal of personalized medicine · 2022Review
- RGS5 Determines Neutrophil Migration in the Acute Inflammatory Phase of Bleomycin-Induced Lung Injury.International journal of molecular sciences · 2021Article
- RGS proteins, GRKs, and beta-arrestins modulate G protein-mediated signaling pathways in asthma.Pharmacology & therapeutics · 2021Review
- Unrestrained GαFrontiers in immunology · 2021Article
- RGS4 promotes allergen- and aspirin-associated airway hyperresponsiveness by inhibiting PGE2 biosynthesis.The Journal of allergy and clinical immunology · 2020Article
- Mechanisms of non-type 2 asthma.Current opinion in immunology · 2020Review
- Article
- Paucigranulocytic asthma: Uncoupling of airway obstruction from inflammation.The Journal of allergy and clinical immunology · 2019Review
- Regulator of G protein signaling 5 restricts neutrophil chemotaxis and trafficking.The Journal of biological chemistry · 2018Article
- A bronchoprotective role forAllergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2018Article
- Downregulation of semaphorin 3E promotes hallmarks of experimental chronic allergic asthma.Oncotarget · 2017Article
- Regulator of G-protein signaling 2 repression exacerbates airway hyper-responsiveness and remodeling in asthma.American journal of respiratory cell and molecular biology · 2015Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundAlthough eosinophilic inflammation typifies allergic asthma, it is not a prerequisite for airway hyperresponsiveness (AHR), suggesting that underlying abnormalities in structural cells, such as airway smooth muscle (ASM), contribute to the asthmatic diathesis. Dysregulation of procontractile G protein-coupled receptor (GPCR) signaling in ASM could mediate enhanced contractility.
objectiveWe explored the role of a regulator of procontractile GPCR signaling, regulator of G protein signaling 5 (RGS5), in unprovoked and allergen-induced AHR.
methodsWe evaluated GPCR-evoked Ca(2+) signaling, precision-cut lung slice (PCLS) contraction, and lung inflammation in naive and Aspergillus fumigatus-challenged wild-type and Rgs5(-/-) mice. We analyzed lung resistance and dynamic compliance in live anesthetized mice using invasive plethysmography.
resultsLoss of RGS5 promoted constitutive AHR because of enhanced GPCR-induced Ca(2+) mobilization in ASM. PCLSs from naive Rgs5(-/-) mice contracted maximally at baseline independently of allergen challenge. RGS5 deficiency had little effect on the parameters of allergic inflammation, including cell counts in bronchoalveolar lavage fluid, mucin production, ASM mass, and subepithelial collagen deposition. Unexpectedly, induced IL-13 and IL-33 levels were much lower in challenged lungs from Rgs5(-/-) mice relative to those seen in wild-type mice.
conclusionLoss of RGS5 confers spontaneous AHR in mice in the absence of allergic inflammation. Because it is selectively expressed in ASM within the lung and does not promote inflammation, RGS5 might be a therapeutic target for asthma.
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Registered trials
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.