ArticleAmerican journal of respiratory cell and molecular biology2015
Receptor for advanced glycation end-products regulates lung fluid balance via protein kinase C-gp91(phox) signaling to epithelial sodium channels.
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 18 papers.
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Who cites it
18 citing papers in PubMed, 41 citations in OpenAlex.
- Biochemical-Cellular crosstalk in diabetes: exploring pathways driving microvascular complications.Molecular biology reports · 2026Review
- Relationship of S100 Proteins with Neuroinflammation.Biomolecules · 2025Review
- Verbascoside Protects Gingival Cells against High Glucose-Induced Oxidative Stress via PKC/HMGB1/RAGE/NFκB Pathway.Antioxidants (Basel, Switzerland) · 2021Article
- Response of the ileum transcriptome to probiotic and fructo-oligosaccharides in Taiping chicken.Journal of applied genetics · 2021Article
- HMGB1 Mediates Paraquat-Induced Neuroinflammatory Responses via Activating RAGE Signaling Pathway.Neurotoxicity research · 2020Article
- High-mobility group box-1 increases epithelial sodium channel activity and inflammation via the receptor for advanced glycation end products.American journal of physiology. Cell physiology · 2020Article
- Redox Signaling and Advanced Glycation Endproducts (AGEs) in Diet-Related Diseases.Antioxidants (Basel, Switzerland) · 2020Review
- Protective effect ofBioscience reports · 2019Article
- Inhibition of the Receptor for Advanced Glycation End-Products in Acute Respiratory Distress Syndrome: A Randomised Laboratory Trial in Piglets.Scientific reports · 2019Article
- Helicobacter Pylori Infection and Lung Cancer: New Insights and Future Challenges.Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2018Review
- 4'-Methoxyresveratrol Alleviated AGE-Induced Inflammation via RAGE-Mediated NF-κB and NLRP3 Inflammasome Pathway.Molecules (Basel, Switzerland) · 2018Article
- RAGE-induced changes in the proteome of alveolar epithelial cells.Journal of proteomics · 2018Article
- Hydrogen Peroxide Stimulates Exosomal Cathepsin B Regulation of the Receptor for Advanced Glycation End-Products (RAGE).Journal of cellular biochemistry · 2018Article
- RAGE inhibition reduces acute lung injury in mice.Scientific reports · 2017Article
- Cytokine-Ion Channel Interactions in Pulmonary Inflammation.Frontiers in immunology · 2017Review
- RAGE Expression and ROS Generation in Neurons: Differentiation versus Damage.Oxidative medicine and cellular longevity · 2016Review
- A Pathophysiologic Approach to Biomarkers in Acute Respiratory Distress Syndrome.Disease markers · 2016Review
- Inhibition of ENaC by endothelin-1.Vitamins and hormones · 2015Review
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
The receptor for advanced glycation end-products (RAGE), a multiligand member of the Ig family, may play a crucial role in the regulation of lung fluid balance. We quantified soluble RAGE (sRAGE), a decoy isoform, and advanced glycation end-products (AGEs) from the bronchoalveolar lavage fluid of smokers and nonsmokers, and tested the hypothesis that AGEs regulate lung fluid balance through protein kinase C (PKC)-gp91(phox) signaling to the epithelial sodium channel (ENaC). Human bronchoalveolar lavage samples from smokers showed increased AGEs (9.02 ± 3.03 μg versus 2.48 ± 0.53 μg), lower sRAGE (1,205 ± 292 pg/ml versus 1,910 ± 263 pg/ml), and lower volume(s) of epithelial lining fluid (97 ± 14 ml versus 133 ± 17 ml). sRAGE levels did not predict ELF volumes in nonsmokers; however, in smokers, higher volumes of ELF were predicted with higher levels of sRAGE. Single-channel patch clamp analysis of rat alveolar epithelial type 1 cells showed that AGEs increased ENaC activity measured as the product of the number of channels (N) and the open probability (Po) (NPo) from 0.19 ± 0.08 to 0.83 ± 0.22 (P = 0.017) and the subsequent addition of 4-hydroxy-2, 2, 6, 6-tetramethylpiperidine-N-oxyl decreased ENaC NPo to 0.15 ± 0.07 (P = 0.01). In type 2 cells, human AGEs increased ENaC NPo from 0.12 ± 0.05 to 0.53 ± 0.16 (P = 0.025) and the addition of 4-hydroxy-2, 2, 6, 6-tetramethylpiperidine-N-oxyl decreased ENaC NPo to 0.10 ± 0.03 (P = 0.013). Using molecular and biochemical techniques, we observed that inhibition of RAGE and PKC activity attenuated AGE-induced activation of ENaC. AGEs induced phosphorylation of p47(phox) and increased gp91(phox)-dependent reactive oxygen species production, a response that was abrogated with RAGE or PKC inhibition. Finally, tracheal instillation of AGEs promoted clearance of lung fluid, whereas concomitant inhibition of RAGE, PKC, and gp91(phox) abrogated the response.
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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.