ArticleThe Journal of biological chemistry2015
Targeted Disruption of Ig-Hepta/Gpr116 Causes Emphysema-like Symptoms That Are Associated with Alveolar Macrophage Activation.
Article in The Journal of biological chemistry, 2015. 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, 27 citations in OpenAlex.
- Adhesion G protein-coupled receptors.Pharmacological reviews · 2026Review
- Anti-Inflammatory Potential of Novel Tethered Agonists of the Adhesion G Protein-Coupled Receptor F5.International journal of molecular sciences · 2026Article
- GPR116 alleviates acetaminophen-induced liver injury in mice by inhibiting endoplasmic reticulum stress.Cellular and molecular life sciences : CMLS · 2024Article
- Molecular changes underlying pulmonary emphysema and chronic bronchitis in Chronic Obstructive Pulmonary Disease: An updated review.Histology and histopathology · 2024Review
- The adhesion-GPCR ADGRF5 fuels breast cancer progression by suppressing the MMP8-mediated antitumorigenic effects.Cell death & disease · 2024Article
- The adhesion GPCR GPR116/ADGRF5 has a dual function in pancreatic islets regulating somatostatin release and islet development.Communications biology · 2024Article
- GPR116 promotes ferroptosis in sepsis-induced liver injury by suppressing system XcCell biology and toxicology · 2023Article
- The clinical relevance of the adhesion G protein-coupled receptor F5 for human diseases and cancers.Biochimica et biophysica acta. Molecular basis of disease · 2023Review
- Article
- Adhesion G protein-coupled receptors: structure, signaling, physiology, and pathophysiology.Physiological reviews · 2022Review
- Identification ofPathogens (Basel, Switzerland) · 2021Article
- Adhesion-GPCR Gpr116 (ADGRF5) expression inhibits renal acid secretion.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- A novel zebrafish model to emulate lung injury by folate deficiency-induced swim bladder defectiveness and protease/antiprotease expression imbalance.Scientific reports · 2019Article
- Loss of the adhesion G-protein coupled receptor ADGRF5 in mice induces airway inflammation and the expression of CCL2 in lung endothelial cells.Respiratory research · 2019Article
- Surfactant Protein D in Respiratory and Non-Respiratory Diseases.Frontiers in medicine · 2018Review
- Article
- Gpr116 Receptor Regulates Distinctive Functions in Pneumocytes and Vascular Endothelium.PloS one · 2015Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ig-Hepta/GPR116 is a member of the G protein-coupled receptor family predominantly expressed in the alveolar type II epithelial cells of the lung. Previous studies have shown that Ig-Hepta is essential for lung surfactant homeostasis, and loss of its function results in high accumulation of surfactant lipids and proteins in the alveolar space. Ig-Hepta knock-out (Ig-Hepta(-/-)) mice also exhibit emphysema-like symptoms, including accumulation of foamy alveolar macrophages (AMs), but its pathogenic mechanism is unknown. Here, we show that the bronchoalveolar lavage fluid obtained from Ig-Hepta(-/-) mice contains high levels of inflammatory mediators, lipid hydroperoxides, and matrix metalloproteinases (MMPs), which are produced by AMs. Accumulation of reactive oxygen species was observed in the AMs of Ig-Hepta(-/-) mice in an age-dependent manner. In addition, nuclear factor-κB (NF-κB) is activated and translocated into the nuclei of the AMs of Ig-Hepta(-/-) mice. Release of MMP-2 and MMP-9 from the AMs was strongly inhibited by treatment with inhibitors of oxidants and NF-κB. We also found that the level of monocyte chemotactic protein-1 is increased in the embryonic lungs of Ig-Hepta(-/-) mice at 18.5 days postcoitum, when AMs are not accumulated and activated. These results suggest that Ig-Hepta plays an important role in regulating macrophage immune responses, and its deficiency leads to local inflammation in the lung, where AMs produce excessive amounts of reactive oxygen species and up-regulate MMPs through the NF-κB signaling pathway.
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