Research Paper Volume 12, Issue 13 pp 12850—12868
Glycosylation end products mediate damage and apoptosis of periodontal ligament stem cells induced by the JNK-mitochondrial pathway
- 1 Affiliated Hospital of Zunyi Medical University, Guizhou, China
- 2 Zunyi Medical University, Department of Periodontology, Stomatological Hospital Zunyi, Guizhou, China
- 3 Chronic Disease Control of Shenzhen, Shenzhen, Guangdong, China
- 4 Third Military Medical University Daping Hospital and Research Institute of Surgery, Stomatology Chongqing, Sichuan, China
- 5 Zunyi Medical University, School of Basic Medical Sciences Zunyi, Guizhou, China
- 6 Department of Stomatology Pingxiang People’s Hospital Pingxiang, JiangXi, China
Received: December 1, 2019 Accepted: March 30, 2020 Published: June 30, 2020https://doi.org/10.18632/aging.103304
How to Cite
Copyright © 2020 Fang et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Background: Recent studies have confirmed the bidirectional relationship between the two and the exacerbation of periodontitis by type II diabetes mellitus (T2DM), the pathogenic mechanism has not yet been clarified, AGEs has been linked to the pathogenesis of both periodontitis and T2DM, JNK signaling pathway might play a important role to explain the inner mechanism.
Objectives: To study advanced glycation end products (AGEs) activate the innate immune system of the host by activating oxidative stress and affecting cellular signal transduction in periodontal ligament stem cells (PDLSCs);
Results: TNF-α and/or AGEs can induce the formation of endogenous ROS in PDLSCs, thereby activating the downstream JNK signalling pathway, leading to the initiation of the mitochondria-mediated apoptotic pathway and the induction of PDLSC apoptosis.
Conclusion: we hypothesized that the JNK pathway is a key link in the apoptosis of PDLSCs mediated by TNF-α and/or AGEs.
Materials and Methods: PDLSCs from healthy volunteers were extracted, cultured and stimulated with TNF-a and/or AGEs, Flow cytometry, CCK-8, multidifferential assay, RT-PCR, apoptosis assay, Transmission electron microscopy and Western blotting were recruit to detect the internal relations between AGEs and PDLSCs.
T2DM: Type 2 diabetes mellitus; PDLSCs: periodontal ligament stem cells; AGEs: advanced glycation end products; ROS: reactive oxygen species; JNK: Jun N-terminal kinase; ALP: alkaline phosphatase.