ArticleMolecular medicine reports2016
NFAT5 participates in seawater inhalation‑induced acute lung injury via modulation of NF-κB activity.
Article in Molecular medicine reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- NFAT5 Regulates IL8 to Promote Cell Growth and Migration in Non-Small Cell Lung Cancer.Thoracic cancer · 2025Article
- Microglial NFAT5 aggravates neuroinflammation via mediating NLRP6 inflammasome in experimental ischemic stroke.Genes & diseases · 2025Article
- Article
- NFAT5: a stress-related transcription factor with multiple functions in health and disease.Cell stress · 2025Review
- Role of environmental pollutants-induced ferroptosis in pulmonary diseases.Frontiers in medicine · 2025Review
- TonEBP: A Key Transcription Factor in Microglia Following Intracerebral Hemorrhage Induced-Neuroinflammation.International journal of molecular sciences · 2024Article
- Vaporization of perfluorocarbon attenuates sea-water-drowning-induced acute lung injury by deactivating the NLRP3 inflammasomes in canines.Experimental biology and medicine (Maywood, N.J.) · 2024Article
- Ganoderic Acid A Alleviates OVA-Induced Asthma in Mice.Inflammation · 2021Article
- Selective inhibition of JNK mitochondrial location is protective against seawater inhalation‑induced ALI/ARDS.Molecular medicine reports · 2021Article
- Amelioration of Lipopolysaccharide-Induced Nephrotic Proteinuria by NFAT5 Depletion Involves Suppressed NF-κB Activity.Inflammation · 2019Article
- Regulation of Inflammatory Functions of Macrophages and T Lymphocytes by NFAT5.Frontiers in immunology · 2019Review
- Anti-inflammatory Role of Pilose Antler Peptide in LPS-Induced Lung Injury.Inflammation · 2017Article
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Authors and funding
9 authors.
Funding
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Abstract
Nuclear factor of activated T cells 5 (NFAT5) is a transcription factor that can be activated by extracellular tonicity. It has been reported that NFAT5 may increase the transcription of certain osmoprotective genes in the renal system, and the aim of the current study was to explore the role of NFAT5 in seawater inhalation‑induced acute lung injury. Though establishing the model of seawater inhalation‑induced acute lung injury, it was demonstrated that seawater inhalation enhanced the transcription and protein expression of NFAT5 (evaluated by reverse transcription‑polymerase chain reaction, immunohistochemistry stain and western blotting) and activation of nuclear factor (NF)‑κB (evaluated by western blotting and mRNA expression levels of three NF‑κB‑dependent genes) both in lung tissue and rat alveolar macrophage cells (NR8383 cells). When expression of NFAT5 was reduced in NR8383 cells using an siRNA targeted to NFAT5, the phosphorylation of NF‑κB and transcription of NF‑κB‑dependent genes were significantly reduced. In addition, the elevated content of certain inflammatory cytokines [tumor necrosis factor α, interleukin (IL)‑1 and IL‑8] were markedly reduced. In conclusion, NFAT5 serves an important pathophysiological role in seawater inhalation‑induced acute lung injury by modulating NF‑κB activity, and these data suggest that NFAT5 may be a promising therapeutic target.
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