ArticleJournal of molecular histology2025
Porphyromonas gingivalis induced DNA oxidative stress damage by iron overload to deplete CTCF expression and prevent osteogenic differentiation of periodontal ligament stem cells.
Article in Journal of molecular histology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
We aimed to investigate the effects of Porphyromonas gingivalis (P. gingivalis) on DNA oxidative damage and osteogenic differentiation of periodontal ligament stem cells (PDLSCs) mediated by iron overload, with special attention to the role of CCCTC-binding factor (CTCF). PDLSCs were co-cultured with different concentrations of P. gingivalis-derived LPS. In addition, deferoxamine (DFO, an iron chelator) or recombinant CTCF protein were used to co-treat PDLSCs. Western blot, immunofluorescence staining, flow cytometry and transmission electron microscopy (TEM) were used to observe the iron overload mediated DNA oxidative damage in PDLSCs. Osteogenic differentiation was assessed based on alkaline phosphatase (ALP) activity, mineralization nodule formation, and bone-related protein expression. CTCF was down-regulated in the gingival tissue of periodontitis patients. P. gingivalis-derived LPS significantly decreased the viability of PDLSCs and suppressed CTCF protein expression, particularly at high concentrations (1 μg/mL 10 μg/mL P. gingivalis-derived LPS). However, co-treatment with DFO alleviated these effects by up-regulating CTCF expression and reducing intracellular iron levels, lipid peroxidation, and DNA damage. Furthermore, P. gingivalis-derived LPS inhibited osteogenic differentiation by decreasing ALP activity, mineralization, and expression levels of bone-associated proteins Runx2, BMP2, BMP4, OPN, and OCN. However, this inhibition was significantly reversed by recombinant CTCF treatment. Our findings underscore the detrimental impact of P. gingivalis on PDLSCs through the suppression of CTCF and highlight the potential therapeutic role of DFO and CTCF in preserving PDLSC function and osteogenic potential.
Indexed as
Identifiers
40455363What OpenQuestion holds
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.