Wnt5a up-regulates Periostin through CaMKII pathway to influence periodontal tissue destruction in early periodontitis
- PMID: 33904122
- DOI: 10.1007/s10735-021-09975-z
Wnt5a up-regulates Periostin through CaMKII pathway to influence periodontal tissue destruction in early periodontitis
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.
References
-
- Abe T, Hajishengallis G (2013) Optimization of the ligature-induced periodontitis model in mice. J Immunol Methods 394:49–54. https://doi.org/10.1016/j.jim.2013.05.002 - DOI - PubMed - PMC
-
- Ailiang Z, Shuanghua H, Xiaoliang S, Lianghua D, Xinnan B, Neng W (2014) Wnt5a promotes migration of human osteosarcoma cells by triggering a phosphatidylinositol-3 kinase/Akt signals. Cancer Cell Int 14:15. https://doi.org/10.1186/1475-2867-14-15 - DOI
-
- Aral CA, Koseoglu S, Saglam M, Pekbagriyanik T, Savran L (2016) Gingival crevicular fluid and salivary periostin levels in non-smoker subjects with chronic and aggressive periodontitis : periostin levels in chronic and aggressive periodontitis. Inflammation 39:986–993. https://doi.org/10.1007/s10753-016-0328-0 - DOI - PubMed
-
- Arslan R, Karsiyaka Hendek M, Kisa U, Olgun E (2020) The effect of non-surgical periodontal treatment on gingival crevicular fluid periostin levels in patients with gingivitis and periodontitis. Oral Dis 00:1–9. https://doi.org/10.1111/odi.13664 - DOI
-
- Balli U, Keles ZP, Avci B, Guler S, Cetinkaya BO, Keles GC (2015) Assessment of periostin levels in serum and gingival crevicular fluid of patients with periodontal disease. J Periodontal Res 50:707–713. https://doi.org/10.1111/jre.12254 - DOI - PubMed
MeSH terms
Substances
Grants and funding
LinkOut - more resources
Full Text Sources
Other Literature Sources