ArticleScientific reports2020
The PDZ motif peptide of ZO-1 attenuates Pseudomonas aeruginosa LPS-induced airway inflammation.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 25 citations in OpenAlex.
- Article
- Functional Analysis of Membrane-Associated Scaffolding Tight Junction (TJ) Proteins in Tumorigenic Characteristics of B16-F10 Mouse Melanoma Cells.International journal of molecular sciences · 2024Article
- PDZ Peptide of the ZO-1 Protein Significantly Increases UTP-InducedMolecules and cells · 2023Article
- DecreasedPeerJ · 2023Article
- Rapid Synergistic Biofilm Production ofInternational journal of molecular sciences · 2022Article
- Distinct Transcriptional Profile of PDZ Genes after Activation of Human Macrophages and Dendritic Cells.International journal of molecular sciences · 2022Article
- Identification of different proteins binding to Na, K-ATPase α1 in LPS-induced ARDS cell model by proteomic analysis.Proteome science · 2022Article
- C/EBPβ Promotes LPS-Induced IL-1β Transcription and Secretion in Alveolar Macrophages via NOD2 Signaling.Journal of inflammation research · 2022Article
- The Role ofToxins · 2021Review
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pseudomonas aeruginosa is known to play a role in many human diseases. Therefore, examining the negative control mechanisms of tight junction protein ZO-1 on the exotoxin LPS of P. aeruginosa-induced diseases could be critical in the development of novel therapeutics. We found that ZO-1 expression dramatically decreased in inflammatory human lung tissues. Interestingly, PDZ1 deletion of the PDZ domain in the ZO-1 protein dramatically decreased LPS-induced F-actin formation and increased the expression of genes for pro-inflammatory cytokines, but not PDZ2 and PDZ3 of the ZO-1 protein. We also found that the consensus PDZ peptide (based on PDZ1) of ZO-1 down-regulates the expression of pro-inflammatory cytokine genes and F-actin formation; in contrast, the GG24,25AA mutant PDZ peptide cannot control these genes. LPS activates IL-8 secretion extracellularly in a time-dependent manner, while the secretion is inhibited by PDZ peptide. Whereas increased IL-8 secretion by LPS activates the CXCR2 receptor, overexpressed RGS12 negatively regulates LPS-induced CXCR2/IL-8 signaling. The PDZ peptide also decreases LPS-induced inflammatory cell populations, pro-inflammatory cytokine gene expression, and TEER in bronchoalveolar lavage fluid and cultured alveolar macrophages. Collectively, we suggest that the PDZ peptide may be a potential therapeutic for bacteria-induced respiratory diseases.
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