scholarly journals The impact of Wnt signalling and hypoxia on osteogenic and cementogenic differentiation in human periodontal ligament cells

2016 ◽  
Vol 14 (6) ◽  
pp. 4975-4982 ◽  
Author(s):  
Shuigen Li ◽  
Jin Shao ◽  
Yinghong Zhou ◽  
Thor Friis ◽  
Jiangwu Yao ◽  
...  
Marine Drugs ◽  
2021 ◽  
Vol 19 (7) ◽  
pp. 388
Author(s):  
Eun-Nam Kim ◽  
Woguti Yvonne Nabende ◽  
Hyeyoon Jeong ◽  
Dongyup Hahn ◽  
Gil-Saeng Jeong

Currently, periodontitis treatment relies on surgical operations, anti-inflammatory agents, or antibiotics. However, these treatments cause pain and side effects, resulting in a poor prognosis. Therefore, in this study, we evaluated the impact of the compound epiloliolide isolated from Sargassum horneri on the recovery of inflammatory inhibitors and loss of periodontal ligaments, which are essential treatment strategies for periodontitis. Here, human periodontal ligament cells stimulated with PG-LPS were treated with the compound epiloliolide, isolated from S. horneri. In the results of this study, epiloliolide proved the anti-inflammatory effect, cell proliferation capacity, and differentiation potential of periodontal ligament cells into osteoblasts, through the regulation of the PKA/CREB signaling pathway. Epiloliolide effectively increased the proliferation and migration of human periodontal ligament cells without cytotoxicity and suppressed the protein expression of proinflammatory mediators and cytokines, such as iNOS, COX-2, TNF-α, IL-6, and IL-1β, by downregulating NLRP3 activated by PG-LPS. Epiloliolide also upregulated the phosphorylation of PKA/CREB proteins, which play an important role in cell growth and proliferation. It was confirmed that the anti-inflammatory effect in PG-LPS-stimulated large cells was due to the regulation of PKA/CREB signaling. We suggest that epiloliolide could serve as a potential novel therapeutic agent for periodontitis by inhibiting inflammation and restoring the loss of periodontal tissue.


2018 ◽  
Vol 475 (4) ◽  
pp. 775-786 ◽  
Author(s):  
Emma Anders ◽  
Daniel Nebel ◽  
Johannes Westman ◽  
Heiko Herwald ◽  
Bengt-Olof Nilsson ◽  
...  

The protein gC1qR (globular C1q receptor), also named p33, was originally identified as a binding partner of the globular heads of C1q in the complement system. gC1qR/p33 is abundantly expressed in many cell types, but the functional importance of this protein is not completely understood. Here, we investigate the impact of gC1qR/p33 on the production and function of the pathophysiologically important chemokine monocyte chemoattractant protein-1 (MCP-1) and the underlying molecular mechanisms. Knockdown of gC1qR/p33 negatively regulated the production of MCP-1, but had no effect on the expression of transcript for MCP-1 in human periodontal ligament cells, suggesting a translational/post-translational mechanism of action. Laser scanning confocal microscopy showed considerable cytosolic co-localization of gC1qR/p33 and MCP-1, and co-immunoprecipitation disclosed direct physical interaction between gC1qR/p33 and MCP-1. Surface plasmon resonance analysis revealed a high-affinity binding (KD = 10.9 nM) between gC1qR/p33 and MCP-1. Using a transwell migration assay, we found that recombinant gC1qR/p33 enhances MCP-1-induced migration of human THP-1 monocytes, pointing to a functional importance of the interaction between gC1qR/p33 and MCP-1. An in vitro assay revealed a rapid turnover of the MCP-1 protein and that gC1qR/p33 stabilizes MCP-1, hence preventing its degradation. We propose that endogenous gC1qR/p33 physically interacts with MCP-1 causing stabilization of the MCP-1 protein and stimulation of its activity in human periodontal ligament cells, suggesting a novel gC1qR/p33-mediated pro-inflammatory mechanism of action.


2016 ◽  
Vol 118 (4) ◽  
pp. 699-708
Author(s):  
Shinichiro Yoshida ◽  
Naohide Yamamoto ◽  
Naohisa Wada ◽  
Atsushi Tomokiyo ◽  
Daigaku Hasegawa ◽  
...  

2011 ◽  
Vol 27 (2) ◽  
pp. 102-108 ◽  
Author(s):  
Payal Saxena ◽  
Vandana Aditya Pant ◽  
Kulvindar Kaur Wadhwani ◽  
Mahendra Pratap Kashyap ◽  
Saurabh Kumar Gupta ◽  
...  

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