Apelin-APJ axis inhibits TNF-alpha-mediated expression of genes involved in the inflammatory response in periodontal ligament cells

서지정보

· 발행기관 : 대한구강생물학회
· 수록지 정보 : International Journal of Oral Biology / 44권 / 4호
· 저자명 : Gyuseok Lee, Won-Hyun Song, Su-Jin Kim, Young-Gwon Kim, Je-Hwang Ryu

목차

Introduction
Materials and Methods
1. Human gingival tissues
2. Cell culture and stimulation
3. RNA isolation, reverse transcription-polymerasechain reaction, and quantitative real time-PCR
4. Statistical analysis
Results
1. Expression of APLN was downregulated in humangingiva affected with periodontitis
2. Adenoviral overexpression of APLN suppressed theexpression of genes involved in inflammation andtissue degradation in human periodontal ligamentcells
3. Adenoviral overexpression of APLN partiallysuppressed the expression of genes involved ininflammation in human gingival fibroblasts
4. APLN-APJ axis could regulate the expressionof genes involved in inflammation and tissuedegradation in human periodontal ligament cells
Discussion
References

영어초록

Periodontitis is an inflammatory disease of the supportive tissues surrounding the teeth, and is characterized by irreversible destruction of the gingiva, periodontal ligament (PDL), and alveolar bone, which results in the loss of teeth. In the present study, we elucidated the correlation between periodontitis and apelin (APLN), an adipokine and a regulatory peptide, respectively, which are involved in inflammation and bone remodeling. The expression of APLN is negatively correlated with periodontitis progression in gingival tissue. In addition, treatment with TNF-α downregulated the expression of APLN in PDL cells and gingival fibroblasts, indicating the protective role played by APLN against periodontitis progression. The overexpression of APLN or treatment with exogenous APLN suppressed the TNF-α- mediated catabolic gene expression of MMP1, IL6 , and PTGS2 in PDL cells. Moreover, the inhibition of the APLNAPJ axis by ML221, an APJ inhibitor, induced catabolic gene expression in PDL cells. Thus, the results of this study provided evidence to support APLN as a regulatory factor of the inflammatory response during periodontitis.

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