4.4 Article

Transcriptome analysis of human periodontal ligament fibroblasts exposed to Porphyromonas gingivalis LPS

Journal

ARCHIVES OF ORAL BIOLOGY
Volume 110, Issue -, Pages -

Publisher

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.archoralbio.2019.104632

Keywords

RNA-seq; P. gingivalis LPS; hPDLFs; Inflammatory cytokines; Chemokines; MMPs

Funding

  1. National Natural Science Foundation of China [81600873]

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Objective: Porphyromonas gingivalis (P. gingivalis)-derived LPS is a major mediator of inflammation and can promote the resorption of alveolar bone in chronic periodontitis. Although the effect of P. gingivalis LPS on human periodontal ligament fibroblasts (hPDLFs) was already investigated by numerous studies, the change of whole transcriptional profile remains undefined. The aim of this study was to investigate P. gingivalis LPS induced whole transcriptional profile in hPDLFs and the expression of the genes associated with the periodontitis. Materials and methods: RNA-seq was performed on hPDLFs treated with or without P. gingivalis LPS. Moreover, the expression of selected inflammatory cytokines, chemokines and matrix metalloproteinases (MMPs), which contribute to periodontitis, were evaluated by quantitative RT-PCR and further measured by ELISA. Results: We found that an average of 12,752 genes were detected among the different groups, and 1374 differentially expressed genes (DEGs) were identified between groups with or without P. gingivalis LPS stimulation for 24 h. However, only 36 DEGs were examined in hPDLFs exposed to P. gingivalis LPS for 24 h or 72 h. Furthermore, the mRNA levels and concentrations of interleukin 8 (IL-8), IL-6, monocyte chemotactic protein 1 (MCP-1), chemokine (CXC motif) ligand 5 (CXCL5), MMP1 and MMP3 were significantly higher in hPDLFs exposed to P. gingivalis LPS for 24 h compared to the untreated hPDLFs. Conclusions: The entire transcriptional profile of P. gingivalis LPS stimulation of hPDLFs was presented for the first time, which could provide an important basis and experimental direction for further research into the mechanisms of periodontitis.

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