scholarly journals Effects of methanandamide on human periodontal ligament cells

2019 ◽  
Author(s):  
Fengqiu Zhang ◽  
Burcu Özdemir ◽  
Phuong Quynh Nguyen ◽  
Oleh Andrukhov ◽  
Xiaohui Rausch-Fan
Keyword(s):  
Periodontal Ligament ◽  
Cannabinoid Receptors ◽  
Endocannabinoid System ◽  
Periodontal Ligament Cells ◽  
Periodontal Tissue ◽  
Inflammatory Conditions ◽  
Human Periodontal Ligament Cells ◽  
Chemotactic Protein ◽  
Improved Stability ◽  
Porphyromonas Gingivalis Lipopolysaccharide

Abstract Background Endocannabinoid system is involved in the regulation of periodontal tissue homeostasis. Synthetic cannabinoid methanandamide (Meth-AEA) has an improved stability and affinity to cannabinoid receptors compared to its endogenous analogue anandamide. In the present study, we investigated the effect of methanandamide on the production of pro-inflammatory mediators in primary human periodontal ligament cells (hPdLCs). Methods hPdLCs were treated with Meth-AEA for 24 h and resulting production of interleukin (IL)-6, IL-8, and monocyte chemotactic protein (MCP)-1 was measured under normal condition as well as under inflammatory conditions mimicked by the presence of Porphyromonas gingivalis lipopolysaccharide (LPS). Additionally, the effect of Meth-AEA on the proliferation/viability of hPdLCs was measured by MTT method. Results Methanandamide at concentration of 10 µM significantly inhibited P. gingivalis LPS induced production of IL-6, IL-8, and MCP-1. Basal production of IL-6 and IL-8 was slightly enhanced by 10 µM Meth-AEA. No effect of Meth-AEA on the basal production of MCP-1 was observed. Proliferation/viability of hPdLCs was not affected by Meth-AEA in concentrations up to 10 µM and was significantly inhibited by 30 µM Meth-AEA. Conclusion Our study supports the influence of cannabinoid system on the inflammatory processes in periodontal tissue and its potential involvement in the progression of periodontal disease.

scholarly journals Methanandamide diminish the Porphyromonas gingivalis lipopolysaccharide induced response in human periodontal ligament cells

2020 ◽  
Author(s):  
Fengqiu Zhang ◽  
Burcu Özdemir ◽  
Phuong Quynh Nguyen ◽  
Oleh Andrukhov ◽  
Xiaohui Rausch-Fan
Keyword(s):  
Porphyromonas Gingivalis ◽  
Periodontal Ligament ◽  
Cannabinoid Receptors ◽  
Endocannabinoid System ◽  
Periodontal Ligament Cells ◽  
Induced Response ◽  
Human Periodontal Ligament Cells ◽  
Chemotactic Protein ◽  
Improved Stability ◽  
Porphyromonas Gingivalis Lipopolysaccharide

Abstract Background: The endocannabinoid system is involved in the regulation of periodontal tissue homeostasis. Synthetic cannabinoid methanandamide (Meth-AEA) has improved stability and affinity to cannabinoid receptors compared to its endogenous analog anandamide. In the present study, we investigated the effect of methanandamide on the production of pro-inflammatory mediators in primary human periodontal ligament cells (hPdLCs).Methods: hPdLCs were treated with Meth-AEA for 24 h, and the resulting production of interleukin (IL)-6, IL-8, and monocyte chemotactic protein (MCP)-1 was measured in the absence or the presence of Porphyromonas gingivalis lipopolysaccharide (LPS). Additionally, the effect of Meth-AEA on the proliferation/viability of hPdLCs was measured by MTT method. Results: Methanandamide at a concentration of 10 µM significantly inhibited P. gingivalis LPS induced production of IL-6, IL-8, and MCP-1. Basal production of IL-6 and IL-8 was slightly enhanced by 10 µM Meth-AEA. No effect of Meth-AEA on the basal production of MCP-1 was observed. Meth-AEA in concentrations up to 10 µM did not affect the proliferation of hPdLCs, but significantly inhibited it at a concentration of 30 µM. Conclusion: Our study suggests that the inflammatory response in periodontal ligament cells could be influenced by the activation of the cannabinoid system, which might be potentially involved in the progression of periodontal disease.

Expression of thymosin beta-4 in human periodontal ligament cells and mouse periodontal tissue and its role in osteoblastic/cementoblastic differentiation

2015 ◽  
Vol 90 (1-3) ◽  
pp. 16-26 ◽  
Author(s):  
Sang-Im Lee ◽  
Deok-Won Lee ◽  
Hyung-Mun Yun ◽  
Hee-Jae Cha ◽  
Cheol-Hyeon Bae ◽  
...  
Keyword(s):  
Periodontal Ligament ◽  
Periodontal Ligament Cells ◽  
Periodontal Tissue ◽  
Thymosin Beta 4 ◽  
Human Periodontal Ligament Cells

LncRNA TUG1 mediates lipopolysaccharide-induced proliferative inhibition and apoptosis of human periodontal ligament cells by sponging miR-132

2019 ◽  
Author(s):  
Ying Han ◽  
Fang Wang ◽  
Longquan Shao ◽  
Peidi Huang ◽  
Yue Xu
Keyword(s):  
Cell Proliferation ◽  
Periodontal Ligament ◽  
Noncoding Rna ◽  
Biological Properties ◽  
Periodontal Ligament Cells ◽  
Inhibition Of Proliferation ◽  
Inflammatory Reactions ◽  
Inflammatory Conditions ◽  
Human Periodontal Ligament Cells ◽  
Proliferation And Apoptosis

Abstract Emerging evidence shows that the long noncoding RNA taurine-upregulated gene 1 (TUG1) plays pivotal roles in regulating biological properties and functions of parenchyma cells in various types of disease processes. However, the mechanism underlying the effects of TUG1 on cell proliferation and apoptosis of human periodontal ligament cells (PDLCs) in periodontitis is undefined. In this study, we explored the functions of TUG1 and its underlying mechanisms in the inflammatory process induced by Porphyromonas gingivalis–derived lipopolysaccharide (LPS) in PDLCs. Our results showed that TUG1 had a decreased expression in both periodontal ligament (PDL) tissues with periodontitis and PDLCs under a LPS-induced inflammatory condition, and TUG1 expression was negatively correlated with miR-132 expression in periodontitis-affected PDL tissues. Furthermore, we found that TUG1 overexpression in PDLCs alleviated LPS-induced proliferative inhibition and apoptosis promotion, while TUG1 knockdown had the opposite effect. In addition, miR-132 inhibitor alleviated TUG1 knockdown-induced inhibition of proliferation and increase of apoptosis in PDLCs under inflammatory conditions induced by LPS. These findings indicated that TUG1 has an enormous potential in regulating cell proliferation and apoptosis of PDLCs during periodontitis and may provide an effective therapeutic target for periodontitis to reduce the damage caused by inflammatory reactions.

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