ArticleInflammation2014
RAGE/NF-κB pathway mediates lipopolysaccharide-induced inflammation in alveolar type I epithelial cells isolated from neonate rats.
Article in Inflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- NDRG1 aggravates Sepsis-Induced acute lung injury via PKM2-dependent activation of STAT3 and NF-κB signaling.BMC immunology · 2026Article
- Inflammation and coagulation abnormalities via the activation of the HMGB1‑RAGE/NF‑κB and F2/Rho pathways in lung injury induced by acute hypoxia.International journal of molecular medicine · 2023Article
- Role of gut microbiota in the modulation of the health effects of advanced glycation end‑products (Review).International journal of molecular medicine · 2023Review
- The AGE-RAGE Axis and RAGE Genetics in Chronic Obstructive Pulmonary Disease.Clinical reviews in allergy & immunology · 2021Review
- Upregulation of Matrix Metalloproteinase-9 Protects against Sepsis-Induced Acute Lung Injury via Promoting the Release of Soluble Receptor for Advanced Glycation End Products.Oxidative medicine and cellular longevity · 2021Article
- Vanillic Acid, a Bioactive Phenolic Compound, Counteracts LPS-Induced Neurotoxicity by Regulating c-Jun N-Terminal Kinase in Mouse Brain.International journal of molecular sciences · 2020Article
- Involvement of Receptor for Advanced Glycation Endproducts in Hypertensive Disorders of Pregnancy.International journal of molecular sciences · 2019Article
- Alveolar-Capillary Membrane-Related Pulmonary Cells as a Target in Endotoxin-Induced Acute Lung Injury.International journal of molecular sciences · 2019Review
- RAGE Plays a Role in LPS-Induced NF-κB Activation and Endothelial Hyperpermeability.Sensors (Basel, Switzerland) · 2017Article
- Primary graft dysfunction: pathophysiology to guide new preventive therapies.Expert review of respiratory medicine · 2017Review
- RAGE/NF-κB signaling mediates lipopolysaccharide induced acute lung injury in neonate rat model.International journal of clinical and experimental medicine · 2015Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alveolar type I epithelial cells (AECIs) play an important role in the pathogenesis of acute lung injury. The receptor for advanced glycation end-products (RAGEs) is expressed at a high basal level in AECIs, and its soluble isoform is suggested as a marker of AECI injury. However, the molecular mechanism by which RAGE mediates inflammatory injury in AECIs remains elusive. In this study, we established lipopolysaccharide (LPS)-induced inflammation in AECIs isolated from neonate rats as the experimental model and investigated the role of RAGE/NF-κB signaling in mediating inflammatory response in AECIs. We found that LPS increased RAGE expression and the secretion of tumor necrosis factor alpha (TNF-α) and interleukin-1 beta (IL-1β) in AECIs in a dose-dependent manner. Knockdown of RAGE significantly decreased TNF-α and IL-1β levels in conditioned medium of AECIs. Electrophoretic mobility shift assay (EMSA) showed that NF-κB activation was increased in AECIs treated by LPS. However, knockdown of RAGE inhibited both basic and LPS-induced NF-κB activity in AECIs. Finally, NF-κB inhibitor pyrrolidine dithiocarbamate (PDTC) significantly reduced LPS-induced upregulation of RAGE expression at both protein and messenger RNA (mRNA) levels in AECIs. Our results suggest that RAGE mediates inflammatory response in AECIs via activating NF-κB, and RAGE/NF-κB pathway presents potential target for the prevention and therapy of acute lung injury.
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