ArticlePloS one2015
Gpr97 Is Dispensable for Inflammation in OVA-Induced Asthmatic Mice.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- KCNJ2 is Required for NLRP3 Inflammasome Activation That Drives Allergic Airway Inflammation and Remodeling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Identification of diagnostic biomarkers of and immune cell infiltration analysis in bovine respiratory disease.Frontiers in veterinary science · 2025Article
- Role of Adhesion G Protein-Coupled Receptors in Immune Dysfunction and Disorder.International journal of molecular sciences · 2023Review
- Article
- Gpr97 Exacerbates AKI by Mediating Sema3A Signaling.Journal of the American Society of Nephrology : JASN · 2018Article
- Resveratrol Attenuates Allergic Asthma and Associated Inflammation in the Lungs Through Regulation of miRNA-34a That Targets FoxP3 in Mice.Frontiers in immunology · 2018Article
- The Adhesion G Protein-Coupled Receptor GPR97/Frontiers in immunology · 2018Article
- Co-inhalation of roflumilast, rather than formoterol, with fluticasone more effectively improves asthma in asthmatic mice.Experimental biology and medicine (Maywood, N.J.) · 2017Article
- P2Y6 contributes to ovalbumin-induced allergic asthma by enhancing mast cell function in mice.Oncotarget · 2016Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAsthma is a complex inflammatory disorder involving the activation and invasion of various immune cells. GPR97 is highly expressed in some immunocytes, including mast cells and eosinophils, which play critical roles in asthma development. However, the role of Gpr97 in regulating airway inflammation in asthma has rarely been reported. In this study, we investigated the potential role of Gpr97 in the development of allergic asthma in mice.
methodsRelevant airway asthmatic mouse models were constructed with both wild-type and Gpr97-/- mice sensitized to 250 μg ovalbumin (OVA). The levels of interleukin IL-4, IL-6 and IFN-γ, which are involved in OVA-induced asthma, in the bronchoalveolar lavage fluid (BALF) and the IgE level in the serum were examined by enzyme-linked immunosorbent assay (ELISA). The invasion of mast cells and eosinophils into lung tissues was assessed by immunohistochemical and eosinophil peroxidase activity assays, respectively. Goblet cell hyperplasia and mucus production were morphologically evaluated with periodic acid-Schiff (PAS) staining.
resultsIn our study, no obvious alteration in the inflammatory response or airway remodeling was found in the Gpr97-deficient mice with OVA-induced asthma. Neither the secretion of cytokines, including IL-4, IL-6 and IFN-γ, nor inflammatory cell recruitment was altered in the Gpr97-deficient mice. Moreover, Gpr97 deficiency did not affect airway remodeling or mucus production in the asthma mouse model.
conclusionOur findings imply that Gpr97 might not be required for the development of airway inflammation in OVA-induced allergic asthma in mice.
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