The vicious circle between mitochondrial oxidative stress and dynamic abnormality mediates triethylene glycol dimethacrylate-induced preodontoblast apoptosis
| Autor: | Wu G, Jianfeng Ma, Yuting Chen, Wang Kh, Shengbin Huang, Xuekun Ren, Xing Jin, Zheng Bb, Xiaoyu Sun, Xiaorong Zhang, Qihao Yu, Yihuai Pan |
|---|---|
| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
Apoptosis Oxidative phosphorylation Mitochondrion medicine.disease_cause Biochemistry Polyethylene Glycols 03 medical and health sciences Mice 0302 clinical medicine stomatognathic system Polymethacrylic Acids Physiology (medical) Dental pulp stem cells medicine Citrate synthase Animals Cells Cultured biology Odontoblasts Chemistry medicine.disease Cell biology Mitochondria Oxidative Stress 030104 developmental biology biology.protein Optic Atrophy 1 Mitochondrial fission Reactive Oxygen Species 030217 neurology & neurosurgery Oxidative stress |
| Zdroj: | Free radical biologymedicine. 134 |
| ISSN: | 1873-4596 |
| Popis: | Oxidative stress (OS) plays crucial roles in triethylene glycol dimethacrylate (TEGDMA, a major component in dental resin)-induced apoptosis of dental pulp cells. Mitochondria are important target organelles for regulating the balance of OS, meanwhile, imbalance of the mitochondrial dynamic associated with mitochondrial dysfunction is one major molecular mechanism for oxidative damages. However, whether these mitochondrial dependent pathways were involved in the apoptosis of dental pulp cells induced by TDGDMA remains unclarified. We demonstrated that TEGDMA decreased viability and induced apoptosis of mouse preodontoblasts (mDPC6T cell line) in a time- and dose-dependent manner. Furthermore, TEGDMA elevated the mitochondrial OS status and induced mitochondrial dysfunction, as reflected by the significant decrease of mitochondrial membrane potential, ATP production, the activity of Complex III and citrate synthase. In this process, we detected a dramatically impaired mitochondrial dynamic that was reflected by significantly enhanced mitochondrial fragmentation. Consistently, we also found a significant enhancement of the key upstream regulators for mitochondrial fission, such as short form of optic atrophy 1, dynamic related protein 1 oligomer and Fission 1. The respective inhibition of mitochondrial OS or mitochondrial fission could mutually attenuate each other, thereby significantly preventing both mitochondrial dysfunction and cell apoptosis. In conclusion, TEGDMA-induced preodontoblasts apoptosis was mediated by the vicious circle between mitochondrial OS and dynamic abnormality, which represented a new target to prevent TEGDMA-induced dental pulp cells apoptosis. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full Text from ScienceDirect