Junchao Liu1, Xiaolin Tang2, Chen Li3, Chunling Pan4, Qian Li5, Fengxue Geng6, Yaping Pan7. 1. Department of Periodontics and Oral Biology, School of Stomatology, China Medical University, Nanjing North Street 117, Shenyang 110002, Liaoning Province, China. Electronic address: cc3092956294@126.com. 2. Department of Periodontics and Oral Biology, School of Stomatology, China Medical University, Nanjing North Street 117, Shenyang 110002, Liaoning Province, China. Electronic address: lin_hope@sina.com. 3. Department of Periodontics and Oral Biology, School of Stomatology, China Medical University, Nanjing North Street 117, Shenyang 110002, Liaoning Province, China. Electronic address: lichen1980716@163.com. 4. Department of Periodontics and Oral Biology, School of Stomatology, China Medical University, Nanjing North Street 117, Shenyang 110002, Liaoning Province, China. Electronic address: chunlingpan@163.com. 5. Department of Periodontics and Oral Biology, School of Stomatology, China Medical University, Nanjing North Street 117, Shenyang 110002, Liaoning Province, China. Electronic address: phebahoney@163.com. 6. Department of Periodontics and Oral Biology, School of Stomatology, China Medical University, Nanjing North Street 117, Shenyang 110002, Liaoning Province, China. Electronic address: gfx1989_@126.com. 7. Department of Periodontics and Oral Biology, School of Stomatology, China Medical University, Nanjing North Street 117, Shenyang 110002, Liaoning Province, China. Electronic address: yppan@mail.cmu.edu.cn.
Abstract
OBJECTIVE: The infection of Porphyromonas gingivalis (P. gingivalis) modulates host immune-inflammatory responses and destructs homeostasis of normal cell cycle, thereby leading to periodontal tissue destruction. Human periodontal ligament fibroblasts (PDLFs) are key players in the host immune responses and periodontal tissue regeneration. The aim of the present study was to discover the effects of P. gingivalis infection on the cell cycle and inflammatory cytokine production in PDLFs. DESIGN: P. gingivalis infection model into PDLFs was established. The effect of P. gingivalis on the cell proliferation and cell cycle were detected by MTT and flow cytometry. The p21, cyclin D1 and cyclin E mRNA expression, p21 protein expression, as well as IL-6 and IL-8 protein levels were analyzed by RT-qPCR, Western blot and ELISA, respectively. RESULTS: P. gingivalis promoted proliferation and G1 phase of PDLFs. G1 phase promotion was associated with the decreased level of p21 and the up-regulation of cyclin D1 at 6h, and with the increased level of cyclin E at 12h. Simultaneously, the immune-inflammatory response of PDLFs was initiated by P. gingivalis during the initial stage of infection, including the increased expressions of IL-6 and IL-8. CONCLUSION: We confirmed that the infection of P. gingivalis could modulate the expression of PDLF genes, which control cell cycle and inflammatory cytokine production. Thus, P. gingivalis may contribute to the proliferation and inflammation of periodontal tissue.
OBJECTIVE: The infection of Porphyromonas gingivalis (P. gingivalis) modulates host immune-inflammatory responses and destructs homeostasis of normal cell cycle, thereby leading to periodontal tissue destruction. Human periodontal ligament fibroblasts (PDLFs) are key players in the host immune responses and periodontal tissue regeneration. The aim of the present study was to discover the effects of P. gingivalis infection on the cell cycle and inflammatory cytokine production in PDLFs. DESIGN: P. gingivalis infection model into PDLFs was established. The effect of P. gingivalis on the cell proliferation and cell cycle were detected by MTT and flow cytometry. The p21, cyclin D1 and cyclin E mRNA expression, p21 protein expression, as well as IL-6 and IL-8 protein levels were analyzed by RT-qPCR, Western blot and ELISA, respectively. RESULTS:P. gingivalis promoted proliferation and G1 phase of PDLFs. G1 phase promotion was associated with the decreased level of p21 and the up-regulation of cyclin D1 at 6h, and with the increased level of cyclin E at 12h. Simultaneously, the immune-inflammatory response of PDLFs was initiated by P. gingivalis during the initial stage of infection, including the increased expressions of IL-6 and IL-8. CONCLUSION: We confirmed that the infection of P. gingivalis could modulate the expression of PDLF genes, which control cell cycle and inflammatory cytokine production. Thus, P. gingivalis may contribute to the proliferation and inflammation of periodontal tissue.
Authors: Livia Aparecida Procópio Gomes; Lívia Mara Alves Figueiredo; Ana Luiza do Rosário Palma; Barbara Maria Corrêa Geraldo; Kelly Cristine Isler Castro; Luciana Ruano de Oliveira Fugisaki; Antônio Olavo Cardoso Jorge; Luciane Dias de Oliveira; Juliana Campos Junqueira Journal: ScientificWorldJournal Date: 2016-09-07