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Erschienen in: Inflammation Research 9/2018

14.07.2018 | Original Research Paper

Role of Ku70 in the apoptosis of inflamed dental pulp stem cells

verfasst von: Yequan Huang, Weiwei Qiao, Xinhuan Wang, Qian Gao, Yao Peng, Zhuan Bian, Liuyan Meng

Erschienen in: Inflammation Research | Ausgabe 9/2018

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Abstract

Aim

The study aimed to investigate the effects of DNA repair proteins on cell apoptosis in human DPSCs during inflammation.

Methods

Lipopolysaccharide (LPS) was used to stimulate inflammation in dental pulp in vivo and in vitro. We identified the activation of DSB response and DNA repair proteins in inflamed pulp tissue and in LPS-treated human DPSCs. Then we transfected the cells with Ku70 (a key protein involved in NHEJ) siRNA and detected the expression changes of γ-H2A.X, DNA repair proteins and cell apoptosis.

Results

Immunohistochemical staining showed that at 4 and 6 days of pulpitis the expression of Ku70 and γ-H2A.X significantly increased. The levels of γ-H2A.X, Ku70, Xrcc4, and Rad51 increased considerably in the LPS-treated DPSCs. Furthermore, decreased expression of Ku70 could increase the number of γ-H2A.X foci, apoptotic cells and reduce cell viability in DPSCs.

Conclusions

The results indicate that NHEJ pathway was the main mechanism involved in DNA damage response induced by repeated LPS stimulation in DPSCs. Meanwhile, the findings suggested that Ku70 serves importantly in the apoptosis of DPSCs in the inflammatory environment.
Literatur
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Zurück zum Zitat Miyashita T, Reed JC. Tumor-suppressor P53 is a direct transcriptional activator of the human bax gene. Cell. 1995;80(2):293–9.CrossRefPubMed Miyashita T, Reed JC. Tumor-suppressor P53 is a direct transcriptional activator of the human bax gene. Cell. 1995;80(2):293–9.CrossRefPubMed
Metadaten
Titel
Role of Ku70 in the apoptosis of inflamed dental pulp stem cells
verfasst von
Yequan Huang
Weiwei Qiao
Xinhuan Wang
Qian Gao
Yao Peng
Zhuan Bian
Liuyan Meng
Publikationsdatum
14.07.2018
Verlag
Springer International Publishing
Erschienen in
Inflammation Research / Ausgabe 9/2018
Print ISSN: 1023-3830
Elektronische ISSN: 1420-908X
DOI
https://doi.org/10.1007/s00011-018-1167-2

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