scholarly journals Inhibitory effects of aviptadil on the SARS-CoV-2 nsp10/ nsp16 protein complex

2021 ◽  
Author(s):  
Sultan F. Alnomasy ◽  
Bader S. Alotaibi ◽  
Ziyad M. Aldosari ◽  
Ahmed H. Mujamammi ◽  
Pragya Anand ◽  
...  
Keyword(s):  
Human Lung ◽  
Rna Stability ◽  
Protein Translation ◽  
Inhibitory Effect ◽  
Lung Epithelial Cells ◽  
Immune Recognition ◽  
Inhibitory Effects ◽  
Mtase Activity ◽  
Lung Epithelial ◽  
Initial Binding

Abstract Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which emerged in late 2019, causes COVID-19, a disease that has been spreading rapidly worldwide. In human lung epithelial cells and monocytes, RLF-100 (aviptadil) has been found to inhibit the RNA replication machinery of SARS-CoV-2, which includes several non-structural proteins (nsp) that play essential roles in synthesizing and replicating viral RNA. This virus is unique in requiring nsp10 and nsp16 for methyltransferase (MTase) activity. This enzyme is essential for RNA stability, protein translation, and viral ability to escape the host's immune recognition. Therefore, we aimed to use bioinformatics tools to analyze aviptadil's inhibitory effect on the SARS-CoV-2 nsp10/nsp16 complex. We present a comprehensive, in silico-generated picture showing how aviptadil may interact with the nsp complex. Specifically, our model predicts how the initial binding of aviptadil to nsp10 and nsp16 may occur. This knowledge can assist drug development efforts against SARS-CoV-2 by providing more target information against nsp16.

Legionella pneumophila induced microRNA expression in human lung epithelial cells

Pneumologie ◽  
2010 ◽  
Vol 64 (S 03) ◽  
Author(s):  
B Schmeck ◽  
B Dolniak ◽  
I Pollock ◽  
C Schulz ◽  
W Bertrams ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Legionella Pneumophila ◽  
Human Lung ◽  
Microrna Expression ◽  
Lung Epithelial Cells ◽  
Lung Epithelial ◽  
Human Lung Epithelial Cells

scholarly journals Effect of Alpha-1 Antitrypsin on CFTR Levels in Primary Human Airway Epithelial Cells Grown at the Air-Liquid-Interface

Molecules ◽  
2021 ◽  
Vol 26 (9) ◽  
pp. 2639
Author(s):  
Frauke Stanke ◽  
Sabina Janciauskiene ◽  
Stephanie Tamm ◽  
Sabine Wrenger ◽  
Ellen Luise Raddatz ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Human Lung ◽  
Liquid Interface ◽  
Lung Epithelial Cells ◽  
Western Blots ◽  
Mesenchymal Transition ◽  
Protein Levels ◽  
Lung Epithelial ◽  
Cftr Protein ◽  
Air Liquid Interface

The cystic fibrosis transmembrane conductance regulator (CFTR) gene is influenced by the fundamental cellular processes like epithelial differentiation/polarization, regeneration and epithelial–mesenchymal transition. Defects in CFTR protein levels and/or function lead to decreased airway surface liquid layer facilitating microbial colonization and inflammation. The SERPINA1 gene, encoding alpha1-antitrypsin (AAT) protein, is one of the genes implicated in CF, however it remains unknown whether AAT has any influence on CFTR levels. In this study we assessed CFTR protein levels in primary human lung epithelial cells grown at the air-liquid-interface (ALI) alone or pre-incubated with AAT by Western blots and immunohistochemistry. Histological analysis of ALI inserts revealed CFTR- and AAT-positive cells but no AAT-CFTR co-localization. When 0.5 mg/mL of AAT was added to apical or basolateral compartments of pro-inflammatory activated ALI cultures, CFTR levels increased relative to activated ALIs. This finding suggests that AAT is CFTR-modulating protein, albeit its effects may depend on the concentration and the route of administration. Human lung epithelial ALI cultures provide a useful tool for studies in detail how AAT or other pharmaceuticals affect the levels and activity of CFTR.

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