ArticleBMC microbiology2006
Temporal activation of anti- and pro-apoptotic factors in human gingival fibroblasts infected with the periodontal pathogen, Porphyromonas gingivalis: potential role of bacterial proteases in host signalling.
Article in BMC microbiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 29 papers.
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
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 74 citations in OpenAlex.
- A review of the roles of pathogens in Alzheimer's disease.Frontiers in neuroscience · 2024Review
- Porphyromonas gingivalis infection alters Nrf2-phase II enzymes and nitric oxide in primary human aortic endothelial cells.Journal of periodontology · 2021Article
- Review
- Article
- Article
- MicroRNA-663 antagonizes apoptosis antagonizing transcription factor to induce apoptosis in epithelial cells.Apoptosis : an international journal on programmed cell death · 2019Article
- New Insights Into the Pathogenesis of Alzheimer's Disease.Frontiers in neurology · 2019Review
- Article
- Dual action of bacteriocin PLNC8 αβ through inhibition of Porphyromonas gingivalis infection and promotion of cell proliferation.Pathogens and disease · 2017Article
- Plant-derived pectin nanocoatings to prevent inflammatory cellular response of osteoblasts followingInternational journal of nanomedicine · 2017Article
- Healthy and Inflamed Gingival Fibroblasts Differ in Their Inflammatory Response to Porphyromonas gingivalis Lipopolysaccharide.Inflammation · 2016Article
- Attenuation of the phosphatidylinositol 3-kinase/Akt signaling pathway by Porphyromonas gingivalis gingipains RgpA, RgpB, and Kgp.The Journal of biological chemistry · 2015Article
- Hydrogen peroxide-induced apoptosis in human gingival fibroblasts.International journal of clinical and experimental pathology · 2015Article
- Porphyromonas gingivalis HmuY stimulates expression of Bcl-2 and Fas by human CD3+ T cells.BMC microbiology · 2013Article
- Integrin α5β1-fimbriae binding and actin rearrangement are essential for Porphyromonas gingivalis invasion of osteoblasts and subsequent activation of the JNK pathway.BMC microbiology · 2013Article
- Host-bacteria crosstalk at the dentogingival junction.International journal of dentistry · 2012Article
- Multiple functional domains and complexes of the two nonstructural proteins of human respiratory syncytial virus contribute to interferon suppression and cellular location.Journal of virology · 2011Article
- Dichotomy of gingipains action as virulence factors: from cleaving substrates with the precision of a surgeon's knife to a meat chopper-like brutal degradation of proteins.Periodontology 2000 · 2010Review
- Oral malodorous compound activates mitochondrial pathway inducing apoptosis in human gingival fibroblasts.Clinical oral investigations · 2010Article
- Bacterial invasion of epithelial cells and spreading in periodontal tissue.Periodontology 2000 · 2010Review
Corrections and comments
- Retraction · 2019-10-17Duplication of/in Image · Manipulation of Images ·
- Retracted
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundPorphyromonas gingivalis is the foremost oral pathogen of adult periodontitis in humans. However, the mechanisms of bacterial invasion and the resultant destruction of the gingival tissue remain largely undefined.
resultsWe report host-P. gingivalis interactions in primary human gingival fibroblast (HGF) cells. Quantitative immunostaining revealed the need for a high multiplicity of infection for optimal infection. Early in infection (2-12 h), P. gingivalis activated the proinflammatory transcription factor NF-kappa B, partly via the PI3 kinase/AKT pathway. This was accompanied by the induction of cellular anti-apoptotic genes, including Bfl-1, Boo, Bcl-XL, Bcl2, Mcl-1, Bcl-w and Survivin. Late in infection (24-36 h) the anti-apoptotic genes largely shut down and the pro-apoptotic genes, including Nip3, Hrk, Bak, Bik, Bok, Bax, Bad, Bim and Moap-1, were activated. Apoptosis was characterized by nuclear DNA degradation and activation of caspases-3, -6, -7 and -9 via the intrinsic mitochondrial pathway. Use of inhibitors revealed an anti-apoptotic function of NF-kappa B and PI3 kinase in P. gingivalis-infected HGF cells. Use of a triple protease mutant P. gingivalis lacking three major gingipains (rgpA rgpB kgp) suggested a role of some or all these proteases in myriad aspects of bacteria-gingival interaction.
conclusionThe pathology of the gingival fibroblast in P. gingivalis infection is affected by a temporal shift from cellular survival response to apoptosis, regulated by a number of anti- and pro-apoptotic molecules. The gingipain group of proteases affects bacteria-host interactions and may directly promote apoptosis by intracellular proteolytic activation of caspase-3.
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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.