Receptor-Interacting Protein 3/Caspase-8 May Regulate Inflammatory Response and Promote Tissue Regeneration in the Periodontal Microenvironment
Bingbing Yan, Kewen Wei, Lipeng Hou, Taiqiang Dai, Yongchun Gu, Xinyu Qiu, Jiangwei Chen, Yuan Feng, Haode Cheng, Zhuo Yu, Yizhe Zhang, Hongmei Zhang, Dehua Li
State Key Laboratory of Military Stomatology and National Clinical Research Center for Oral Diseases and Shaanxi Engineering Research Center for Dental Materials and Advanced Manufacture, Department of Oral Implants, School of Stomatology, The Fourth Military Medical University, Xi’an, Shaanxi, China (mainland)
Med Sci Monit 2018; 24: LBR5247-5257
Available online: 2018-07-29
Periodontal ligament stem cells (PDLSCs) possess characteristics of multi-potential differentiation and immuno-modulation, and PDLSCs-mediated periodontal tissue regeneration is regarded as a hopeful method for periodontitis treatment. Recent studies demonstrated that RIP3 and caspase8 regulate bacteria-induced innate immune response and programmed necrosis, which is also called necroptosis. This study aimed to determine the role of the RIP3/Caspase8 signal pathway on necroptosis of PDLSCs under the inflammatory microenvironment, both in vitro and in vivo.
MATERIAL AND METHODS: PDLSCs were cultured, and transmission electron microscopy and flow cytometry were used to detect necroptosis. PCR, ALP, and Alizarin Red S staining were used to assess the effect of necroptosis on osteogenesis differentiation of PDLSCs in vitro, while HE and Masson staining were taken after the nude mouse subcutaneous transplant experiment.
RESULTS: Our research indicates that RIP3/caspase8 can regulate the immune response of PDLSCs, and blockade of RIP3/caspase8 can protect the biological characteristics of the PDLSCs, effectively promoting periodontal tissue regeneration in the inflammatory microenvironment.
CONCLUSIONS: Inhibiting RIP3/caspase8 can effectively promote periodontal tissue regeneration in the inflammatory microenvironment.
Keywords: Necrosis, Periodontal Ligament, periodontitis, Receptor-Interacting Protein Serine-Threonine Kinases