Human β-defensin 3 gene modification promotes the osteogenic differentiation of human periodontal ligament cells and bone repair in periodontitis.
10.1038/s41368-020-0078-6
- Author:
Lingjun LI
1
;
Han JIANG
2
;
Rixin CHEN
1
;
Jing ZHOU
3
,
4
;
Yin XIAO
5
;
Yangheng ZHANG
6
;
Fuhua YAN
7
Author Information
1. Nanjing Stomatological Hospital, Medical School of Nanjing University, Nanjing, China.
2. People's Hospital of Suzhou National New & Hi-Tech Industrial Development Zone, Suzhou, China.
3. The Affiliated Stomatological Hospital, Zhejiang University School of Medicine
4. Key Laboratory of Oral Biomedical Research of Zhejiang Province, Zhejiang University School of Stomatology, Hangzhou, China.
5. Institute of Health and Biomedical Innovation & the Australia-China Centre for Tissue Engineering and Regenerative Medicine, Queensland University of Technology, Brisbane, Australia.
6. Nanjing Stomatological Hospital, Medical School of Nanjing University, Nanjing, China. zhangyh207@163.com.
7. Nanjing Stomatological Hospital, Medical School of Nanjing University, Nanjing, China. yanfh@nju.edu.cn.
- Publication Type:Journal Article
- MeSH:
Animals;
Anti-Infective Agents;
metabolism;
pharmacology;
Cell Differentiation;
drug effects;
Cells, Cultured;
Humans;
Osteogenesis;
drug effects;
Periodontal Ligament;
drug effects;
metabolism;
Periodontitis;
drug therapy;
Rats;
Rats, Sprague-Dawley;
beta-Defensins;
metabolism;
pharmacology
- From:
International Journal of Oral Science
2020;12(1):13-13
- CountryChina
- Language:English
-
Abstract:
Efforts to control inflammation and achieve better tissue repair in the treatment of periodontitis have been ongoing for years. Human β-defensin 3, a broad-spectrum antimicrobial peptide has been proven to have a variety of biological functions in periodontitis; however, relatively few reports have addressed the effects of human periodontal ligament cells (hPDLCs) on osteogenic differentiation. In this study, we evaluated the osteogenic effects of hPDLCs with an adenoviral vector encoding human β-defensin 3 in an inflammatory microenvironment. Then human β-defensin 3 gene-modified rat periodontal ligament cells were transplanted into rats with experimental periodontitis to observe their effects on periodontal bone repair. We found that the human β-defensin 3 gene-modified hPDLCs presented with high levels of osteogenesis-related gene expression and calcium deposition. Furthermore, the p38 MAPK pathway was activated in this process. In vivo, human β-defensin 3 gene-transfected rat PDLCs promoted bone repair in SD rats with periodontitis, and the p38 mitogen-activated protein kinase (MAPK) pathway might also have been involved. These findings demonstrate that human β-defensin 3 accelerates osteogenesis and that human β-defensin 3 gene modification may offer a potential approach to promote bone repair in patients with periodontitis.
