ArticleAmerican journal of physiology. Lung cellular and molecular physiology2014
Regulation of epithelial sodium channels in urokinase plasminogen activator deficiency.
Article in American journal of physiology. Lung cellular and molecular physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Meta-Analysis of Preclinical Studies of Fibrinolytic Therapy for Acute Lung Injury.Frontiers in immunology · 2018Pooled it
- Alveolar Type 2 Epithelial Cell Organoids: Focus on Culture Methods.Biomedicines · 2023Review
- Article
- PAI-1 regulates AT2-mediated re-alveolarization and ion permeability.Stem cell research & therapy · 2023Article
- Fibrinolytic system and COVID-19: From an innovative view of epithelial ion transport.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2023Review
- PAI-1 regulates AT2-mediated re-alveolarization and ion permeability.Research square · 2023Article
- Competitive cleavage of SARS-CoV-2 spike protein and epithelial sodium channel by plasmin as a potential mechanism for COVID-19 infection.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- ENaC activation by proteases.Acta physiologica (Oxford, England) · 2022Review
- Recent Advances in Nanomaterials for Diagnosis, Treatments, and Neurorestoration in Ischemic Stroke.Frontiers in cellular neuroscience · 2022Review
- Fibrinolytic or anti-plasmin (nafamostat) therapy for COVID-19: A timing challenge for clinicians.Pulmonary pharmacology & therapeutics · 2021Article
- Ion transport mechanisms for smoke inhalation-injured airway epithelial barrier.Cell biology and toxicology · 2020Article
- Plasmin improves blood-gas barrier function in oedematous lungs by cleaving epithelial sodium channels.British journal of pharmacology · 2020Article
- Article
- The Effect of CaInternational journal of molecular sciences · 2018Article
- Ion channels of the lung and their role in disease pathogenesis.American journal of physiology. Lung cellular and molecular physiology · 2017Review
- Physiology and pathophysiology of the plasminogen system in the kidney.Pflugers Archiv : European journal of physiology · 2017Review
- The function and regulation of acid-sensing ion channels (ASICs) and the epithelial Na(+) channel (ENaC): IUPHAR Review 19.British journal of pharmacology · 2016Review
- CPT-cGMP Is A New Ligand of Epithelial Sodium Channels.International journal of biological sciences · 2016Review
- Article
- Role of epithelial sodium channels in the regulation of lung fluid homeostasis.American journal of physiology. Lung cellular and molecular physiology · 2015Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Epithelial sodium channels (ENaC) govern transepithelial salt and fluid homeostasis. ENaC contributes to polarization, apoptosis, epithelial-mesenchymal transformation, etc. Fibrinolytic proteases play a crucial role in virtually all of these processes and are elaborated by the airway epithelium. We hypothesized that urokinase-like plasminogen activator (uPA) regulates ENaC function in airway epithelial cells and tested that possibility in primary murine tracheal epithelial cells (MTE). Both basal and cAMP-activated Na(+) flow through ENaC were significantly reduced in monolayers of uPA-deficient cells. The reduction in ENaC activity was further confirmed in basolateral membrane-permeabilized cells. A decrease in the Na(+)-K(+)-ATPase activity in the basolateral membrane could contribute to the attenuation of ENaC function in intact monolayer cells. Dysfunctional fluid resolution was seen in uPA-disrupted cells. Administration of uPA and plasmin partially restores ENaC activity and fluid reabsorption by MTEs. ERK1/2, but not Akt, phosphorylation was observed in the cells and lungs of uPA-deficient mice. On the other hand, cleavage of γ ENaC is significantly depressed in the lungs of uPA knockout mice vs. those of wild-type controls. Expression of caspase 8, however, did not differ between wild-type and uPA(-/-) mice. In addition, uPA deficiency did not alter transepithelial resistance. Taken together, the mechanisms for the regulation of ENaC by uPA in MTEs include augmentation of Na(+)-K(+)-ATPase, proteolysis, and restriction of ERK1/2 phosphorylation. We demonstrate for the first time that ENaC may serve as a downstream signaling target by which uPA controls the biophysical profiles of airway fluid and epithelial function.
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