ArticleBiomedicine & pharmacotherapy = Biomedecine & pharmacotherapie2022
Ursodeoxycholic acid ameliorates cell migration retarded by the SARS-CoV-2 spike protein in BEAS-2B human bronchial epithelial cells.
Article in Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 33 citations in OpenAlex.
- Pathogen-Specific Regulation of Renin-Angiotensin System Genes in Epithelial Cells: A Comparative Study of SARS-CoV-2 Spike Protein N-Terminal Domain Fragment and Bacterial Lipopolysaccharide.Pathogens (Basel, Switzerland) · 2026Article
- Ursodeoxycholic acid inhibits pneumonia caused by PRCV through the activation of TLR4-IRF3 mediated type Ⅰ interferon pathway.Veterinary research · 2026Article
- Ursodeoxycholic Acid Attenuates B Cell Susceptibility to SARS-CoV-2 Spike Protein by Interfering Its Binding to ACE2.Biomolecules & therapeutics · 2025Article
- SARS-CoV-2 spike treatment and transfection impairs airway epithelial repair.ERJ open research · 2025Article
- Ursodeoxycholic acid relieves clinical severity of COVID-19 in patients with chronic liver diseases.Frontiers in medicine · 2025Article
- The Role of Ursodeoxycholic Acid Administration During the COVID-19 Pandemic: A Questionnaire Survey.The Canadian journal of infectious diseases & medical microbiology = Journal canadien des maladies infectieuses et de la microbiologie medicale · 2025Article
- Ursodeoxycholic acid and severe COVID-19 outcomes in a cohort study using the OpenSAFELY platform.Communications medicine · 2024Article
- Insights into SARS-CoV-2: Small-Molecule Hybrids for COVID-19 Treatment.Molecules (Basel, Switzerland) · 2024Review
- Association Between Ursodeoxycholic Acid and Clinical Outcomes in Patients With COVID-19 Infection: Population-Based Cohort Study.JMIR public health and surveillance · 2024Article
- Review
- Interplay between Bile Acids and Intestinal Microbiota: Regulatory Mechanisms and Therapeutic Potential for Infections.Pathogens (Basel, Switzerland) · 2024Review
- The Value of Ursodeoxycholic Acid and Mesenchymal Stem Cells in the Treatment of Severe COVID-19.Microorganisms · 2024Article
- Bile acids and coronavirus disease 2019.Acta pharmaceutica Sinica. B · 2024Review
- Dihydroartemisinin-Ursodeoxycholic Bile Acid Hybrids in the Fight against SARS-CoV-2.ACS omega · 2023Article
- Invasive FoxM1 phosphorylated by PLK1 induces the polarization of tumor-associated macrophages to promote immune escape and metastasis, amplified by IFITM1.Journal of experimental & clinical cancer research : CR · 2023Article
- Development of HPLC-CAD method for simultaneous quantification of nine related substances in ursodeoxycholic acid and identification of two unknown impurities by HPLC-Q-TOF-MS.Journal of pharmaceutical and biomedical analysis · 2023Article
- A perspective study of the possible impact of obeticholic acid against SARS-CoV-2 infection.Inflammopharmacology · 2023Review
- Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCoronavirus disease 2019 (COVID-19) is caused by severe acute -respiratory syndrome coronavirus 2 (SARS- CoV-2) through interaction of the spike protein (SP) with the receptor-binding domain (RBD) and its receptor, angiotensin converting enzyme 2(ACE2). Repair mechanisms induced following virus infection can restore the protective barrier through wound healing. Then, cells from the epithelial basal layer repopulate the damaged area, followed by cell proliferation and differentiation, as well as changes in gene expression.
methodsUsing Beas-2B cells and SP, we investigated whether ursodeoxycholic acid (UDCA) contributes to restoration of the bronchial epithelial layer. ACE2 expression was measured by RT-PCR and Western blotting. SP-ACE2 interaction was analyzed by flow cytometry and visualized through immunostaining. Cell migration was assessed using single cell path tracking and wound healing assay.
resultsUpon ACE2 overexpression in HeLa, HEK293T, and Beas-2B cells following the transfection of pCMV-ACE2 plasmid DNA, SP binding on each cell was increased in the ACE2 overexpression group compared to pCMV-transfected control cells. SP treatment delayed the migration of BEAS-2B cells compared to the control. SP also reduced cell migration, even under ACE2 overexpression; SP binding was greater in ACE2-overexpressed cells than control cells. UDCA interfered significantly with the binding of SP to ACE2 under our experimental conditions. UDCA also restored the inhibitory migration of Beas-2B cells induced by SP treatment. CONCLSION: Our data demonstrate that UDCA can contribute to the inhibition of abnormal airway epithelial cell migration. These results suggest that UDCA can enhance the repair mechanism, to prevent damage caused by SP-ACE2 interaction and enhance restoration of the epithelial basal layer.
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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.