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Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils
Published on: January 21, 2020
Modulation of Wnt5a expression by periodontopathic bacteria
Hiromi Nanbara1, Nawarat Wara-aswapati, Toshiyuki Nagasawa
1Department of Periodontology, Tokyo Medical and Dental University, Tokyo, Japan.
Plos One
|April 10, 2012
Summary
Wingless protein 5a (Wnt5a) is upregulated in periodontitis and its expression is modulated by P. gingivalis lipopolysaccharide via NF-κB and STAT1 pathways. This suggests Wnt5a as a potential therapeutic target for periodontal inflammation.
Area of Science:
- Oral biology
- Immunology
- Molecular biology
Background:
- Wingless (Wnt) proteins regulate development, immunity, and disease.
- Wnt5a signaling is crucial for macrophage inflammatory responses.
- Periodontitis involves chronic inflammation and bone loss driven by bacteria.
Purpose of the Study:
- To investigate Wnt5a expression in periodontitis tissue.
- To elucidate the molecular mechanisms of Wnt5a regulation by P. gingivalis lipopolysaccharide (LPS).
Main Methods:
- RT-PCR to measure Wnt5a mRNA in human periodontitis tissue and LPS-stimulated THP-1 cells.
- Analysis of NF-κB pathway activation (IκBα degradation, DNA binding).
- Investigating the roles of IFN-γ, STAT1, and TLRs in Wnt5a induction.
Main Results:
- Wnt5a mRNA was significantly upregulated in chronic periodontitis tissues compared to healthy controls.
- P. gingivalis LPS induced Wnt5a expression in THP-1 cells, more so than E. coli LPS.
- NF-κB pathway activation and STAT1 were critical for P. gingivalis LPS-induced Wnt5a expression, enhanced by IFN-γ.
Conclusions:
- P. gingivalis modulates Wnt5a expression through NF-κB and STAT1 signaling pathways.
- Wnt5a may play a significant role in periodontal inflammation.
- Targeting Wnt5a could offer novel therapeutic strategies for periodontitis.
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