ArticleAmerican journal of translational research2016
Pendrin, an anion exchanger on lung epithelial cells, could be a novel target for lipopolysaccharide-induced acute lung injury mice.
Article in American journal of translational research, 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, 22 citations in OpenAlex.
- The comparison of two pendrin inhibitors, YS-01 and PDSinh-C01, in lipopolysaccharide-induced acute lung injury.Scientific reports · 2026Article
- Pendrin inhibition is associated with protective effect of prone positioning in a ventilator-induced lung injury mouse model.Scientific reports · 2025Article
- Solute Carrier Family 26 Member 4 (SLC26A4), A Potential Therapeutic Target for Asthma.Journal of respiratory biology and translational medicine · 2024Article
- Chloride/Multiple Anion Exchanger SLC26A Family: Systemic Roles of SLC26A4 in Various Organs.International journal of molecular sciences · 2024Review
- Mechanism of anion exchange and small-molecule inhibition of pendrin.Nature communications · 2024Article
- Methazolamide Reduces the AQP5 mRNA Expression and Immune Cell Migration-A New Potential Drug in Sepsis Therapy?International journal of molecular sciences · 2024Article
- Inhibition of the sodium-dependent HCOeLife · 2022Article
- Static Stretch Increases the Pro-Inflammatory Response of Rat Type 2 Alveolar Epithelial Cells to Dynamic Stretch.Frontiers in physiology · 2022Article
- Inhibition of Pendrin by a small molecule reduces Lipopolysaccharide-induced acute Lung Injury.Theranostics · 2020Article
- Inflammation and Monocyte Recruitment due to Aging and Mechanical Stretch in Alveolar Epithelium are Inhibited by the Molecular Chaperone 4-phenylbutyrate.Cellular and molecular bioengineering · 2018Article
- Expression of trans-membrane serine protease 3 (TMPRSS3) in the human organ of Corti.Cell and tissue research · 2018Article
- Lipopolysaccharide-induced CCN1 production enhances interleukin-6 secretion in bronchial epithelial cells.Cell biology and toxicology · 2018Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThe aim of this study is to evaluate the role of pendrin in acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) and to explore whether pendrin expression existing on alveolar cells.
methodsALI C57BL/6 mice model induced by lipopolysaccharide (LPS) was established. The expression of pendrin in lung was analyzed by RT-PCR and western blotting methods, the changes of lung inflammatory parameters and pathology were observed, the cellular distribution of pendrin in the lung was determined using immunofluorescence. Statistical comparisons between groups were made by two-tailed Student's t-test.
resultsEnhanced expression of the slc26a4 gene and production of pendrin in lungs of LPS-induced ALI mice were confirmed. In comparison with vehicle-control mice, methazolamide treatment mitigated lung inflammatory parameters and pathology. IL-6 and MCP-1 in lung tissues and BALF in methazolamide-treated mice were statistically decreased. Methazolamide treatment had significant effect on the total protein concentration in the BALF and the ratio of lung wet/dry weight. The percentage of macrophages in the BALF was increased. There was a low expression of pendrin in ATII.
conclusionsPendrin may be involved in pathological process of LPS-induced ALI. Inhibition of the pendrin function could be used to treat ALI. Airway epithelial cell may be a valuable therapeutic target for discovering and developing new drugs and/or new therapeutic strategies for the treatment of ALI/ARDS.
Indexed as
Identifiers
27158384PMC4846941W2400570514What OpenQuestion holds
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.