ArticleCellular microbiology2015
FOXO responses to Porphyromonas gingivalis in epithelial cells.
Article in Cellular microbiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
37 citing papers in PubMed, 45 citations in OpenAlex.
- Molecular Regulation of FOXO1 and Its Pathophysiological Significance in Endometriosis: A Narrative Review.Antioxidants (Basel, Switzerland) · 2025Review
- Oral Microbiota and Carcinogenesis: Exploring the Systemic Impact of Oral Pathogens.Pathogens (Basel, Switzerland) · 2025Review
- The Role of Reactive Oxygen Species (ROS) in Periodontitis: A Potential Therapeutic Target.Immunity, inflammation and disease · 2025Review
- Anti-Inflammatory Properties of Yellow Passion Fruit Bagasse Extract and Its Potential Role in Periodontal Wound Healing In Vitro.Biomedicines · 2025Article
- FLLL31 Induces Apoptosis via the FOXO4/BCL6 Axis to Inhibit Bladder Cancer Progression.Human mutation · 2025Article
- Delineation of global, absolutely essential and conditionally essential pangenomes of Porphyromonas gingivalis.Scientific reports · 2024Article
- About a Possible Impact of Endodontic Infections byInternational journal of molecular sciences · 2024Review
- Review
- Illuminating the oral microbiome: cellular microbiology.FEMS microbiology reviews · 2023Article
- Anti‑tumor properties of FoxO1 in YD‑9 oral squamous cell carcinoma cells.Oncology reports · 2023Article
- Role of Porphyromonas gingivalis in oral and orodigestive squamous cell carcinoma.Periodontology 2000 · 2022Review
- Targeting Nrf2 with Probiotics and Postbiotics in the Treatment of Periodontitis.Biomolecules · 2022Review
- RNA Sequencing Reveals the Upregulation of FOXO Signaling Pathway inInternational journal of molecular sciences · 2022Article
- Cathelicidin LL-37 in Health and Diseases of the Oral Cavity.Biomedicines · 2022Review
- Periodontal Pathogens: A Crucial Link Between Periodontal Diseases and Oral Cancer.Frontiers in microbiology · 2022Review
- FOXO1 inhibits FSL-1 regulation of integrin β6 by blocking STAT3 binding to the integrin β6 gene promoter.Frontiers in cellular and infection microbiology · 2022Article
- A bacterial tyrosine phosphatase modulates cell proliferation through targeting RGCC.PLoS pathogens · 2021Article
- Regulation of Anti-Apoptotic SOD2 and BIRC3 in Periodontal Cells and Tissues.International journal of molecular sciences · 2021Article
- The Roles of FOXO1 in Periodontal Homeostasis and Disease.Journal of immunology research · 2021Review
- Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Porphyromonas gingivalis is a prominent periodontal, and emerging systemic, pathogen that redirects host cell signalling pathways and modulates innate immune responses. In this study, we show that P. gingivalis infection induces the dephosphorylation and activation of forkhead box-O (FOXO)1, 3 and 4 in gingival epithelial cells. In addition, immunofluorescence showed that FOXO1 accumulated in the nucleus of P. gingivalis-infected cells. Quantitative reverse transcription PCR demonstrated that transcription of genes involved in protection against oxidative stress (Cat, Sod2, Prdx3), inflammatory responses (IL1β) and anti-apoptosis (Bcl-6) was induced by P. gingivalis, while small-interfering RNA (siRNA)-mediated knockdown of FOXO1 suppressed the transcriptional activation of these genes. P. gingivalis-induced secretion of interleukin (IL)-1β and inhibition of apoptosis were also impeded by FOXO1 knockdown. Neutralization of reactive oxygen species (ROS) by N-acetyl-l-cysteine blocked the activation of FOXO1 by P. gingivalis and concomitantly suppressed the activation of oxidative stress responses, anti-apoptosis programmes and IL-β production. Inhibition of c-Jun-N-terminal kinase (JNK) either pharmacologically or by siRNA, reduced FOXO1 activation and downstream FOXO1-dependent gene regulation in response to P. gingivalis. The results indicate that P. gingivalis-induced ROS activate FOXO transcription factors through JNK signalling, and that FOXO1 controls oxidative stress responses, inflammatory cytokine production and cell survival. These data position FOXO as an important signalling node in the epithelial cell-P. gingivalis interaction, with particular relevance to cell fate and dysbiotic host responses.
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Registered trials
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.