Vasoactive Intestinal Peptide (VIP) in COVID-19 Therapy-Shedding of ACE2 and TMPRSS2 via ADAM10
Patients infected with SARS-CoV-2 may develop mild respiratory symptoms but also Acute Respiratory Distress Syndrome (ARDS). Additionally, severe systemic inflammation contributes to morbidity and mortality. The SARS-CoV-2 virus enters the cell by binding to the angiotensin-converting enzyme 2 (ACE2...
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| Hauptverfasser: | , , , , , , , , , , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
16 March 2025
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| In: |
International journal of molecular sciences
Year: 2025, Jahrgang: 26, Heft: 6, Pages: 114 |
| ISSN: | 14220067 |
| DOI: | 10.3390/ijms26062666 |
| Online-Zugang: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.3390/ijms26062666
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| Verfasserangaben: | Charlotte Gutzler, Kerstin Höhne, Daniele Bani, Gian Kayser, Sebastian Fähndrich, Michael Ambros, Martin J. Hug, Siegbert Rieg, Valeria Falcone, Joachim Müller-Quernheim, Gernot Zissel and Björn C. Frye |
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| 520 | |a Patients infected with SARS-CoV-2 may develop mild respiratory symptoms but also Acute Respiratory Distress Syndrome (ARDS). Additionally, severe systemic inflammation contributes to morbidity and mortality. The SARS-CoV-2 virus enters the cell by binding to the angiotensin-converting enzyme 2 (ACE2) receptor, followed by cleavage by transmembrane serine protease 2 (TMPRSS2). Vasoactive intestinal peptide (VIP) is known for its immune-modulating effects by suppressing the release of pro-inflammatory cytokines and enhancing regulatory T-cells. Furthermore, it has been tested in SARS-CoV-2-related clinical trials. We set out to investigate its role in the setting of SARS-CoV-2 infection in vitro. Epithelial cells (CaCo-2) were stimulated with SARS-CoV-2 spike protein, treated with native VIP and analyzed to investigate the mRNA and surface expression of ACE2 and TMPRSS2, the enzyme activity of TMPRSS2 and the infection rate by a SARS-CoV-2 pseudovirus. VIP downregulated ACE2 and TMPRSS2 mRNA and surface expression. Beyond these direct effects, VIP mediates the shedding of surface-expressed ACE2 and TMPRSS2 via upregulation of a sheddase protease (ADAM10). Functionally, these dual mechanisms of VIP-mediated downregulation of proteins involved in SARS-CoV-2 cell entry resulted in a reduced infection rate by the SARS-CoV-2 pseudovirus. These data imply that VIP hampers viral entry mechanisms based on SARS-CoV-2 and the linkage to ADAM10 may stimulate research in other indications beyond SARS-CoV-2. | ||
| 650 | 4 | |a ACE2 | |
| 650 | 4 | |a ADAM10 Protein | |
| 650 | 4 | |a Amyloid Precursor Protein Secretases | |
| 650 | 4 | |a Angiotensin-Converting Enzyme 2 | |
| 650 | 4 | |a Caco-2 Cells | |
| 650 | 4 | |a COVID-19 | |
| 650 | 4 | |a COVID-19 Drug Treatment | |
| 650 | 4 | |a Humans | |
| 650 | 4 | |a Membrane Proteins | |
| 650 | 4 | |a SARS-CoV-2 | |
| 650 | 4 | |a Serine Endopeptidases | |
| 650 | 4 | |a shedding by ADAM10 | |
| 650 | 4 | |a Spike Glycoprotein, Coronavirus | |
| 650 | 4 | |a TMPRSS2 | |
| 650 | 4 | |a vasoactive intestinal peptide | |
| 650 | 4 | |a Vasoactive Intestinal Peptide | |
| 650 | 4 | |a Virus Internalization | |
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