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. 2024 Jul 23;14:16895. doi: 10.1038/s41598-024-66473-4

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© This is a U.S. Government work and not under copyright protection in the US; foreign copyright protection may apply 2024

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Cardiac glycoside drugs rescue CFTR from loss in differentiated BCi.NS1.1 (d-BCi) epithelia following infection by authentic SARS-CoV-2 virus. (a) Representative Western blot of protein samples collected from differentiated dBCi cells, cultured at the ALI for 28 days, and infected with SARS-CoV-2 (strain β 1.315). Conditions included medium only, virus only, and virus with 50 nM of either digitoxin or ouabain. Heating and disulfide bond breakage are omitted from the protein preparation, leaving the high molecular weight CFTR dimer to be detected. β-actin is used as a loading control. (b) Densitometry analysis was used to determine CFTR/β-actin ratio. Averages ± SD were calculated from N = 4 independent experiments. P values were determined with a one-way ANOVA, followed by a Dunnett’s post-hoc test comparing each mean to the medium control. A significant difference from the medium control was determined only for treatment with spike protein alone (p = 0.0103).