2. Academic Validation
  3. Wnt5a up-regulates Periostin through CaMKII pathway to influence periodontal tissue destruction in early periodontitis

Wnt5a up-regulates Periostin through CaMKII pathway to influence periodontal tissue destruction in early periodontitis

  • J Mol Histol. 2021 Jun;52(3):555-566. doi: 10.1007/s10735-021-09975-z.
Liu Qian 1 2 3 4 5,  Guo Shujuan 6 7 8 9 10,  Huang Ping 3 4 5,  Liu Li 1 2 3 4 5,  Shi Weiwei 1 2 3 4 5,  Wu Yafei 3 4 5,  Tian Weidong 11 12 13 14 15
Affiliations

Affiliations

  • 1 Engineering Research Center of Oral Translational Medicine, Ministry of Education, West China Hospital of Stomatology, Sichuan University, Chengdu, 610041, China.
  • 2 National Engineering Laboratory for Oral Regenerative Medicine, West China Hospital of Stomatology, Sichuan University, Chengdu, 610041, China.
  • 3 State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, 610041, China.
  • 4 National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, 610041, China.
  • 5 Department of Periodontics, West China Hospital of Stomatology, Sichuan University, Chengdu, 610041, China.
  • 6 Engineering Research Center of Oral Translational Medicine, Ministry of Education, West China Hospital of Stomatology, Sichuan University, Chengdu, 610041, China. guo.shujuan@yahoo.com.
  • 7 National Engineering Laboratory for Oral Regenerative Medicine, West China Hospital of Stomatology, Sichuan University, Chengdu, 610041, China. guo.shujuan@yahoo.com.
  • 8 State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, 610041, China. guo.shujuan@yahoo.com.
  • 9 National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, 610041, China. guo.shujuan@yahoo.com.
  • 10 Department of Periodontics, West China Hospital of Stomatology, Sichuan University, Chengdu, 610041, China. guo.shujuan@yahoo.com.
  • 11 Engineering Research Center of Oral Translational Medicine, Ministry of Education, West China Hospital of Stomatology, Sichuan University, Chengdu, 610041, China. drtwd@sina.com.
  • 12 National Engineering Laboratory for Oral Regenerative Medicine, West China Hospital of Stomatology, Sichuan University, Chengdu, 610041, China. drtwd@sina.com.
  • 13 State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, 610041, China. drtwd@sina.com.
  • 14 National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, 610041, China. drtwd@sina.com.
  • 15 Department of Oral and Maxillofacial Surgery, West China Hospital of Stomatology, Sichuan University, Chengdu, 610041, China. drtwd@sina.com.
PMID: 33904122 DOI: 10.1007/s10735-021-09975-z
Abstract

Periostin is essential for periodontal tissue integrity and homeostasis and also associated with periodontitis and periodontitis healing. This study aims to investigate the temporal and spatial expression of Periostin and Wnt5a/CaMKII in periodontitis and how the Wnt5a regulates Periostin through CaMKII signaling pathway in PDLCs in inflammatory environment. The experimental periodontitis mice were adopted to clarify the temporal and spatial expression of Wnt5a, CaMKII and Periostin during early periodontitis. And the Wnt5a, CaMKII and Periostin expression pattern and regulation mechanism in PDLCs were clarified in Porphyromonas gingivalis Lipopolysaccharide (P.g. LPS) induced inflammatory condition. Along with the periodontitis development, Wnt5a, CaMKII and Periostin significantly increased in periodontal ligament and partially increased in gingiva during 0 to 6 day (P < 0.05). They were involved in early periodontitis homeostasis especially in periodontal ligament tissue. Meanwhile, Wnt5a, CaMKII and Periostin were significantly decreased at 12 h (P < 0.05) and increased at 48 h (P < 0.05) in PDLCs after induced by P.g. LPS. Besides, Wnt5a significantly enhanced total CaMKII protein (P < 0.05), pCaMKII (P < 0.001) and Periostin (P < 0.001), and this could be blocked by CaMKII inhibitor KN93 (P < 0.05). In conclusions, in early periodontitis, Wnt5a/CaMKII and Periostin should be involved in maintaining periodontal homeostasis and Wnt5a could up-regulate Periostin via CaMKII pathway in inflammation, which would provide new clues for us to understand the pathogenesis of periodontitis and develop better therapeutic strategies.

Keywords

CaMKII; Inflammatory microenvironment; Periodontitis; Periostin; Wnt5a.

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  • HY-15465
    99.42%, CaMK II Inhibitor‎