ArticleAmerican journal of respiratory cell and molecular biology2015
Regulator of G-protein signaling 2 repression exacerbates airway hyper-responsiveness and remodeling in asthma.
Article in American journal of respiratory cell and molecular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 33 citations in OpenAlex.
- Type 2-low Asthma: Epidemiology, Multiomics, and Emerging Therapies.Current allergy and asthma reports · 2026Review
- Betaine Downregulates RARRES1 to Alleviate Cartilage Fibrosis and Promote Hyaline Cartilage Repair.International journal of molecular sciences · 2026Article
- RGS2 is an innate immune checkpoint for suppressing Gαq-mediated IFNγ generation and lung injury.iScience · 2025Article
- Review
- Synergistic Enhancement of Isoforskolin and Dexamethasone Against Sepsis and Acute Lung Injury Mouse Models.Journal of inflammation research · 2023Article
- Human umbilical cord mesenchymal stem cells combined with pirfenidone upregulates the expression of RGS2 in the pulmonary fibrosis in mice.Respiratory research · 2022Article
- Dual loss of regulator of G protein signaling 2 and 5 exacerbates ventricular myocyte arrhythmias and disrupts the fine-tuning of GJournal of molecular and cellular cardiology · 2022Article
- Clinical and molecular implications of RGS2 promoter genetic variation in severe asthma.The Journal of allergy and clinical immunology · 2022Article
- The pivotal role of the NLRC4 inflammasome in neuroinflammation after intracerebral hemorrhage in rats.Experimental & molecular medicine · 2021Article
- RGS proteins, GRKs, and beta-arrestins modulate G protein-mediated signaling pathways in asthma.Pharmacology & therapeutics · 2021Review
- Airway Epithelial Cells Drive Airway Smooth Muscle Cell Phenotype Switching to the Proliferative and Pro-inflammatory Phenotype.Frontiers in physiology · 2021Article
- Mechanisms of non-type 2 asthma.Current opinion in immunology · 2020Review
- RGS4 Overexpression in Lung Attenuates Airway Hyperresponsiveness in Mice.American journal of respiratory cell and molecular biology · 2018Article
- A bronchoprotective role forAllergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2018Article
- Group 2 Innate Lymphoid Cells Exhibit a Dynamic Phenotype in Allergic Airway Inflammation.Frontiers in immunology · 2017Article
- Understanding how long-acting βBritish journal of pharmacology · 2016Review
- [Effect of triggering receptor expressed on myeloid cells 2 overexpression on airway inflammation and remodeling in mice with allergic asthma].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2016Article
- Upregulation of RGS2: a new mechanism for pirfenidone amelioration of pulmonary fibrosis.Respiratory research · 2016Article
- Airway hyperresponsiveness; smooth muscle as the principal actor.F1000Research · 2016Review
- Regulator of G Protein Signaling 2: A Versatile Regulator of Vascular Function.Progress in molecular biology and translational science · 2015Review
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
Abstract
G protein-coupled receptors (GPCRs) are important regulators of cell functions in asthma. We recently reported that regulator of G-protein signaling (RGS) 2, a selective modulator of Gq-coupled GPCRs, is a key regulator of airway hyper-responsiveness (AHR), the pathophysiologic hallmark of asthma. Because RGS2 protein levels in airway cells were significantly lower in patients with asthma compared with patients without asthma, we further investigated the potential pathological importance of RGS2 repression in asthma. The human RGS2 gene maps to chromosome 1q31. We first screened patients with asthma for RGS2 gene promoter single-nucleotide polymorphisms (SNPs) and found significant differences in the distribution of two RGS2 SNPs (A638G, rs2746071 and C395G, rs2746072) between patients with asthma and nonasthmatic subjects. These two SNPs are always associated with each other and have the same higher prevalence in patients with asthma (65%) as compared with nonasthmatic subjects (35%). Point mutations corresponding to these SNPs decrease RGS2 promoter activity by 44%. The importance of RGS2 down-regulation was then determined in an acute IL-13 mouse model of asthma. Intranasal administration of IL-13 in mice also decreased RGS2 expression in lungs by ∼50% and caused AHR. Although naive RGS2 knockout (KO) mice exhibit spontaneous AHR, acute IL-13 exposure further increased AHR in RGS2 KO mice. Loss of RGS2 also significantly enhanced IL-13-induced mouse airway remodeling, including peribronchial smooth muscle thickening and fibrosis, without effects on goblet cell hyperplasia or airway inflammation in mice. Thus, genetic variations and increased inflammatory cytokines can lead to RGS2 repression, which exacerbates AHR and airway remodeling in 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.