ArticleAmerican journal of respiratory cell and molecular biology2018
LPS-induced Acute Lung Injury Involves NF-κB-mediated Downregulation of SOX18.
Article in American journal of respiratory cell and molecular biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 75 citations in OpenAlex.
- Human chorionic membrane mesenchymal stem cell-conditioned medium activates the SOX18/MECP2 axis to protect against sepsis-induced lung injury.Journal of molecular histology · 2026Article
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- USP7-mediated stabilization of CXCL3 aggravates inflammation in models of acute lung injury.Journal of thoracic disease · 2025Article
- Citri Sarcodactylis Fructus Alleviates LPS-Induced Acute Lung Injury by Inhibiting Inflammation and Inflammasome Activation.Food science & nutrition · 2025Article
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- A systematic review of the research progress of traditional Chinese medicine against pulmonary fibrosis: from a pharmacological perspective.Chinese medicine · 2023Review
- 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
- ISGylation of NF-κBp65 by SCFArteriosclerosis, thrombosis, and vascular biology · 2023Article
- The effects of flaxseed supplementation on concentration of circulating adipokines in patients with ulcerative colitis.Gastroenterology and hepatology from bed to bench · 2023Article
- Protective Effects ofInternational journal of molecular sciences · 2022Article
- Ceramide induces pyroptosis through TXNIP/NLRP3/GSDMD pathway in HUVECs.BMC molecular and cell biology · 2022Article
- Tight Junctions, the Epithelial Barrier, and Toll-like Receptor-4 During Lung Injury.Inflammation · 2022Review
- Caveolin-1 identified as a key mediator of acute lung injury using bioinformatics and functional research.Cell death & disease · 2022Article
- Intense light-elicited alveolar type 2-specific circadian PER2 protects from bacterial lung injury via BPIFB1.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- Fe-Curcumin Nanozyme-Mediated Reactive Oxygen Species Scavenging and Anti-Inflammation for Acute Lung Injury.ACS central science · 2022Article
- Integrated Network Pharmacology and Experimental Validation Approach to Investigate the Therapeutic Effects of Capsaicin on Lipopolysaccharide-Induced Acute Lung Injury.Mediators of inflammation · 2022Article
- Loss of SOX18/CLAUDIN5 disrupts the pulmonary endothelial barrier in ventilator-induced lung injury.Frontiers in physiology · 2022Article
- SOX18-associated gene signature predicts sepsis outcome.American journal of translational research · 2022Article
- Phosphorus dendron nanomicelles as a platform for combination anti-inflammatory and antioxidative therapy of acute lung injury.Theranostics · 2022Article
- NF-κB-dependent repression of Sox18 transcription factor requires the epigenetic regulators histone deacetylases 1 and 2 in acute lung injury.Frontiers in physiology · 2022Article
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Authors and funding
21 authors at 6 institutions in 1 country.
Funding
Abstract
One of the early events in the progression of LPS-mediated acute lung injury in mice is the disruption of the pulmonary endothelial barrier resulting in lung edema. However, the molecular mechanisms by which the endothelial barrier becomes compromised remain unresolved. The SRY (sex-determining region on the Y chromosome)-related high-mobility group box (Sox) group F family member, SOX18, is a barrier-protective protein through its ability to increase the expression of the tight junction protein CLDN5. Thus, the purpose of this study was to determine if downregulation of the SOX18-CLDN5 axis plays a role in the pulmonary endothelial barrier disruption associated with LPS exposure. Our data indicate that both SOX18 and CLDN5 expression is decreased in two models of in vivo LPS exposure (intraperitoneal, intratracheal). A similar downregulation was observed in cultured human lung microvascular endothelial cells (HLMVECs) exposed to LPS. SOX18 overexpression in HLMVECs or in the mouse lung attenuated the LPS-mediated vascular barrier disruption. Conversely, reduced CLDN5 expression (siRNA) reduced the HLMVEC barrier-protective effects of SOX18 overexpression. The mechanism by which LPS decreases SOX18 expression was identified as transcriptional repression through binding of NF-κB (p65) to a SOX18 promoter sequence located between -1,082 and -1,073 bp with peroxynitrite contributing to LPS-mediated NF-κB activation. We conclude that NF-κB-dependent decreases in the SOX18-CLDN5 axis are essentially involved in the disruption of human endothelial cell barrier integrity associated with LPS-mediated acute lung injury.
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