Helicobacter pyloriinhibited cell proliferation in human periodontal ligament fibroblasts through the Cdc25C/CDK1/cyclinB1 signaling cascade
| Autor: | Dongsheng Liang, Wanghong Zhao, Hongmin Zhuang, Naiming Hu, Jianing He, Huanying Li, Xingzhu Dai |
|---|---|
| Rok vydání: | 2019 |
| Předmět: |
0206 medical engineering
02 engineering and technology Cell cycle Periodontal Science Flow cytometry 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Multiplicity of infection medicine Periodontitis Cyclin B1 Cell proliferation Cyclin-dependent kinase 1 Helicobacter pylori medicine.diagnostic_test biology Chemistry Cell growth Tyrosine phosphorylation 030206 dentistry biology.organism_classification 020601 biomedical engineering Molecular biology Periodontics Oral Surgery Research Article Periodontal ligament |
| Zdroj: | Journal of Periodontal & Implant Science |
| ISSN: | 2093-2286 2093-2278 |
| DOI: | 10.5051/jpis.2019.49.3.138 |
| Popis: | Purpose Several studies have shown that the oral cavity is a secondary location for Helicobacter pylori colonization and that H. pylori is associated with the severity of periodontitis. This study investigated whether H. pylori had an effect on the periodontium. We established an invasion model of a standard strain of H. pylori in human periodontal ligament fibroblasts (hPDLFs), and evaluated the effects of H. pylori on cell proliferation and cell cycle progression. Methods Different concentrations of H. pylori were used to infect hPDLFs, with 6 hours of co-culture. The multiplicity of infection in the low- and high-concentration groups was 10:1 and 100:1, respectively. The Cell Counting Kit-8 method and Ki-67 immunofluorescence were used to detect cell proliferation. Flow cytometry, quantitative real-time polymerase chain reaction, and western blots were used to detect cell cycle progression. In the high-concentration group, the invasion of H. pylori was observed by transmission electron microscopy. Results It was found that H. pylori invaded the fibroblasts, with cytoplasmic localization. Analyses of cell proliferation and flow cytometry showed that H. pylori inhibited the proliferation of periodontal fibroblasts by causing G2 phase arrest. The inhibition of proliferation and G2 phase arrest were more obvious in the high-concentration group. In the low-concentration group, the G2 phase regulatory factors cyclin dependent kinase 1 (CDK1) and cell division cycle 25C (Cdc25C) were upregulated, while cyclin B1 was inhibited. However, in the high-concentration group, cyclin B1 was upregulated and CDK1 was inhibited. Furthermore, the deactivated states of tyrosine phosphorylation of CDK1 (CDK1-Y15) and serine phosphorylation of Cdc25C (Cdc25C-S216) were upregulated after H. pylori infection. Conclusions In our model, H. pylori inhibited the proliferation of hPDLFs and exerted an invasive effect, causing G2 phase arrest via the Cdc25C/CDK1/cyclin B1 signaling cascade. Its inhibitory effect on proliferation was stronger in the high-concentration group. Graphical Abstract |
| Databáze: | OpenAIRE |
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