ArticleGene therapy2016
β1-Na(+),K(+)-ATPase gene therapy upregulates tight junctions to rescue lipopolysaccharide-induced acute lung injury.
Article in Gene therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 52 citations in OpenAlex.
- A gene therapy approach to prevent dilated intercellular space, a hallmark of gastroesophageal reflux disease.Gene therapy · 2026Article
- The role of Na,K‑ATPase in lung diseases (Review).Molecular medicine reports · 2025Review
- Enhanced itaconic acid secretion from macrophages mediates the protection of mesenchymal stem cell-derived exosomes on lipopolysaccharide-induced acute lung injury mice.Biology direct · 2024Article
- Retracted article: Protective effects of ulinastatin on rats with acute lung injury induced by lipopolysaccharide.Bioengineered · 2024Article
- Occludin Is Essential to Maintain Normal Alveolar Barrier Integrity and Its Protective Role During ARDS Progression.International journal of molecular sciences · 2024Article
- Protective Effect of Vitamin K2 (MK-7) on Acute Lung Injury Induced by Lipopolysaccharide in Mice.Current issues in molecular biology · 2024Article
- Upregulation of alveolar fluid clearance is not sufficient for NaScientific reports · 2023Article
- The Na/K-ATPase role as a signal transducer in lung inflammation.Frontiers in immunology · 2023Review
- SIRT6 ameliorates LPS-induced apoptosis and tight junction injury in ARDS through the ERK1/2 pathway and autophagy.International journal of medical sciences · 2023Article
- Identification of different proteins binding to Na, K-ATPase α1 in LPS-induced ARDS cell model by proteomic analysis.Proteome science · 2022Article
- Gene transfer of MRCKα rescues lipopolysaccharide-induced acute lung injury by restoring alveolar capillary barrier function.Scientific reports · 2021Article
- Article
- Pulmonary gene delivery-Realities and possibilities.Experimental biology and medicine (Maywood, N.J.) · 2021Review
- Gene Therapy for Acute Respiratory Distress Syndrome.Frontiers in physiology · 2021Review
- Alveolar epithelial glycocalyx shedding aggravates the epithelial barrier and disrupts epithelial tight junctions in acute respiratory distress syndrome.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021Article
- Crocin alleviates lipopolysaccharide-induced acute respiratory distress syndrome by protecting against glycocalyx damage and suppressing inflammatory signaling pathways.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020Article
- Caveolin-1 gene therapy inhibits inflammasome activation to protect from bleomycin-induced pulmonary fibrosis.Scientific reports · 2019Article
- Autophagy regulates the therapeutic potential of adipose-derived stem cells in LPS-induced pulmonary microvascular barrier damage.Cell death & disease · 2019Article
- Mesenchymal stem cells with downregulated Hippo signaling attenuate lung injury in mice with lipopolysaccharide‑induced acute respiratory distress syndrome.International journal of molecular medicine · 2019Article
- Loss of barrier integrity in alveolar epithelial cells downregulates ENaC expression and activity via CaPflugers Archiv : European journal of physiology · 2018Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are associated with diverse disorders and characterized by disruption of the alveolar-capillary barrier, leakage of edema fluid into the lung, and substantial inflammation leading to acute respiratory failure. Gene therapy is a potentially powerful approach to treat ALI/ARDS through repair of alveolar epithelial function. Herein, we show that delivery of a plasmid expressing β1-subunit of the Na(+),K(+)-ATPase (β1-Na(+),K(+)-ATPase) alone or in combination with epithelial sodium channel (ENaC) α1-subunit using electroporation not only protected from subsequent lipopolysaccharide (LPS)-mediated lung injury, but also treated injured lungs. However, transfer of α1-subunit of ENaC (α1-ENaC) alone only provided protection benefit rather than treatment benefit although alveolar fluid clearance had been remarkably enhanced. Gene transfer of β1-Na(+),K(+)-ATPase, but not α1-ENaC, not only enhanced expression of tight junction protein zona occludins-1 (ZO-1) and occludin both in cultured cells and in mouse lungs, but also reduced pre-existing increase of lung permeability in vivo. These results demonstrate that gene transfer of β1-Na(+),K(+)-ATPase upregulates tight junction formation and therefore treats lungs with existing injury, whereas delivery of α1-ENaC only maintains pre-existing tight junction but not for generation. This indicates that the restoration of epithelial/endothelial barrier function may provide better treatment of ALI/ARDS.
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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.