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Updated: Oct 8, 2025
Isolation of Primary Human Decidual Cells from the Fetal Membranes of Term Placentae
Published on: April 30, 2018
Placenta-specific 8 (PLAC8) mediates inflammation and mobility of the hPDLCs via MEK/ERK signaling pathway
Chungang Zhao1, Tingqian Zou2, Ruiping Tang1
1Medical College of Jingchu University of Technology.
Background:
Placenta-specific 8 (PLAC8) is reported to regulate cellular functions in the progression of various diseases. However, its role in periodontitis is still unclear.
Methods:
Human periodontal ligament cells (hPDLCs) were treated with lipopolysaccharide of Porphyromonas Gingivalis (LPS-PG) to mimic periodontitis in vitro. Real-time quantitative polymerase chain reaction (RT-qPCR) was performed to measure the mRNA expression levels and western blot was for protein levels. Wound healing and transwell migration assays were performed to assess the cell mobility of hPDLCs. Both mRNA and protein levels of inflammatory cytokines including IFN-γ, IL-17, TNF-α, IL-4, IL-10 and IL-13 were accessed to evaluated process of periodontitis in vitro. Furthermore, the protein expressions of mitogen-activated protein kinase kinase (MEK), extracellular regulated protein kinase (ERK) and their phosphorylated products quantified by western blotting assay were determined to confirm the activation of the MEK/ERK signaling pathway.
Results:
The microarray analysis results showed that PLAC8 was most significantly downregulated in periodontium samples of patients with periodontitis, which participates in blood coagulation and integrin-mediated signaling pathway. PLAC8 was also markedly downregulated in the LPS-PG-treated hPDLCs. Moreover, overexpression of PLAC8 ameliorated inflammation and promoted cell mobility of LPS-PG-treated hPDLCs, while inhibition of PLAC8 exhibited the opposite effects. MEK/ERK was selected based on analyses of the protein-protein interaction (PPI) network as the potential signaling pathway interacted with PLAC8, and PLAC8 showed regulatory function on activation of the MEK/ERK pathway. Additionally, U0126, the inhibitor of MEK, abrogated the effects of PLAC8 on inflammation and cell mobility of LPS-PG-treated hPDLCs.
Conclusion:
Overexpression of PLAC8 protected hPDLCs from dysfunction of inflammation and cell mobility via activating MEK/ERK pathway, indicating a novel therapeutic target for periodontitis.
Insights
Placenta-specific 8 (PLAC8) is downregulated in periodontitis, where it protects cells from inflammation and promotes mobility by activating the MEK/ERK pathway. This suggests PLAC8 is a potential therapeutic target for periodontitis.
Area of Science:
- Periodontal disease research
- Cellular signaling pathways
- Molecular biology
Background:
- Placenta-specific 8 (PLAC8) regulates cellular functions in disease, but its role in periodontitis is unknown.
- Periodontitis is a significant oral disease with complex cellular mechanisms.
Purpose of the Study:
- To investigate the role of PLAC8 in periodontitis.
- To elucidate the underlying molecular mechanisms, including signaling pathways involved.
Main Methods:
- Human periodontal ligament cells (hPDLCs) were treated with Porphyromonas Gingivalis lipopolysaccharide (LPS-PG) to model periodontitis.
- Gene and protein expression of PLAC8 and inflammatory cytokines were analyzed using RT-qPCR and western blot.
- Cell mobility was assessed via wound healing and transwell assays.
- The MEK/ERK signaling pathway activation was investigated.
Main Results:
- PLAC8 expression was significantly downregulated in periodontitis tissues and LPS-PG-treated hPDLCs.
- Overexpression of PLAC8 reduced inflammation and enhanced cell mobility in LPS-PG-treated hPDLCs.
- PLAC8 demonstrated regulatory control over the MEK/ERK pathway, and its effects on inflammation and mobility were abrogated by a MEK inhibitor.
Conclusions:
- PLAC8 overexpression protects hPDLCs from periodontitis-induced dysfunction by activating the MEK/ERK pathway.
- PLAC8 represents a novel therapeutic target for periodontitis treatment.
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