ArticleCellular microbiology2009
Porphyromonas gingivalis invades human trophoblasts and inhibits proliferation by inducing G1 arrest and apoptosis.
Article in Cellular microbiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
What it found
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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
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.
- [Pathways and Mechanisms of Periodontitis Contributing to Adverse Pregnancy Outcomes].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2023Pooled it
- Macrophage-Hosted Porphyromonas gingivalis Is a Risk Factor for Cataract Development.Investigative ophthalmology & visual science · 2025Article
- Porphyromonas gingivalis-mediated disruption in spiral artery remodeling is associated with altered uterine NK cell populations and dysregulated IL-18 and Htra1.Scientific reports · 2022Article
- Classifying Integrated Signature Molecules in Macrophages of Rheumatoid Arthritis, Osteoarthritis, and Periodontal Disease: An Omics-Based Study.Current issues in molecular biology · 2022Article
- Relationship between IgA Nephropathy andInternational journal of molecular sciences · 2021Article
- Review
- Oral Administration ofInternational journal of molecular sciences · 2019Article
- Article
- Porphyromonas gingivalis strain-dependent inhibition of uterine spiral artery remodeling in the pregnant rat.Biology of reproduction · 2018Article
- Cell Cycle Arrest and Apoptosis Induced by Porphyromonas gingivalis Require Jun N-Terminal Protein Kinase- and p53-Mediated p38 Activation in Human Trophoblasts.Infection and immunity · 2018Article
- Galectin-3 Plays an Important Role in Preterm Birth Caused by Dental Infection of Porphyromonas gingivalis.Scientific reports · 2018Article
- Review
- Oral cancer cells sustainedly infected with Porphyromonas gingivalis exhibit resistance to Taxol and have higher metastatic potential.Oncotarget · 2017Article
- Role of Maternal Periodontitis in Preterm Birth.Frontiers in immunology · 2017Review
- The Periodontal Pathogen Porphyromonas gingivalis Preferentially Interacts with Oral Epithelial Cells in S Phase of the Cell Cycle.Infection and immunity · 2016Article
- Article
- Porphyromonas gingivalis within Placental Villous Mesenchyme and Umbilical Cord Stroma Is Associated with Adverse Pregnancy Outcome.PloS one · 2016Article
- Involvement of protease-activated receptor 4 in over-expression of matrix metalloproteinase 9 induced by Porphyromonas gingivalis.Medical microbiology and immunology · 2015Article
- Porphyromonas gingivalis promotes invasion of oral squamous cell carcinoma through induction of proMMP9 and its activation.Cellular microbiology · 2014Article
- Listeria monocytogenes induces host DNA damage and delays the host cell cycle to promote infection.Cell cycle (Georgetown, Tex.) · 2014Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Porphyromonas gingivalis is an oral pathogen that is also associated with serious systemic conditions such as preterm delivery. Here we investigated the interaction between P. gingivalis and a cell line of extravillous trophoblasts (HTR-8) derived from the human placenta. P. gingivalis internalized within HTR-8 cells and inhibited proliferation through induction of arrest in the G1 phase of the cell cycle. G1 arrest was associated with decreased expression of cyclin D and of CDKs 2, 4 and 6. In addition, levels of CDK inhibitors p15, p16, p18 and p21 were increased following P. gingivalis infection. The amount of Rb was diminished by P. gingivalis, and transient overexpression of Rb, with concomitant upregulation of phospho-Rb, relieved P. gingivalis-induced G1 arrest. HTR-8 cells halted in the G1 phase became apoptotic, and apoptosis was accompanied by an increase in the ratio of Bax/Bcl-2 and increased activity of caspases 3, 7 and 9. HTR-8 cells infected with P. gingivalis also exhibited a sustained activation of ERK1/2, and knock-down of ERK1/2 activity with siRNA abrogated both G1 arrest and apoptosis. Thus, P. gingivalis can invade placental trophoblasts and induce G1 arrest and apoptosis through pathways involving ERK1/2 and its downstream effectors, properties that provide a mechanistic basis for pathogenicity in complications of pregnancy.
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Registered trials
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