Transient receptor potential vanilloid‐1 regulates osteoprotegerin/RANKL homeostasis in human periodontal ligament cells

Sooampon, Sireerat; Manokawinchoke, Jeeranan; Pavasant, Prasit

doi:10.1111/j.1600-0765.2012.01493.x

Cited by 21 publications

(19 citation statements)

References 36 publications

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“…Nevertheless, in our research, we found that blocking TRPV1 in the parodontium could reduce the expression of TRPV1 in the TG. Previous research showed that TRPV1 was present in gingival epithelial cells and periodontal ligament cells, and contributes to the regulation of cell proliferation and protein secretion [24][25]. Furthermore, suppressing TRPV1 also decreased the secretion of IL-1β in the gingival crevicular fluid.…”

Section: Discussionmentioning

confidence: 89%

Blocking of TRPV-1 in the parodontium relieves orthodontic pain by inhibiting the expression of TRPV-1 in the trigeminal ganglion during experimental tooth movement in rats

Gao

Liu

Zhang

et al. 2016

Neuroscience Letters

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Section: Discussionmentioning

confidence: 89%

Blocking of TRPV-1 in the parodontium relieves orthodontic pain by inhibiting the expression of TRPV-1 in the trigeminal ganglion during experimental tooth movement in rats

Gao

Liu

Zhang

et al. 2016

Neuroscience Letters

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“…In addition, AEA but not 2-AG is known to activate transient receptor potential vanilloid type-1 receptor (TRPV1) [41]. Recent study shows that this receptor is expressed in hPdLC and might be activated by AEA [42]. Moreover, ablation of TRPV1 in mice results in exacerbated inflammatory response during endotoxic shock [43], which also suggests the role of this receptor in LPS-induced signaling.…”

Section: Discussionmentioning

confidence: 99%

Endocannabinoids and Inflammatory Response in Periodontal Ligament Cells

et al. 2014

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Endocannabinoids are associated with multiple regulatory functions in several tissues. The main endocannabinoids, anandamide (AEA) and 2-arachidonylglycerol (2-AG), have been detected in the gingival crevicular fluid of periodontitis patients, but the association between periodontal disease or human periodontal ligament cells (hPdLCs) and endocannabinoids still remain unclear. The aim of the present study was to examine the effects of AEA and 2-AG on the proliferation/viability and cytokine/chemokine production of hPdLCs in the presence/absence of Porphyromonas gingivalis lipopolysaccharide (P. gingivalis LPS). The proliferation/viability of hPdLCs was measured using 3,4,5-dimethylthiazol-2-yl-2,5-diphenyl tetrazolium bromide (MTT)-assay. Interleukin-6 (IL-6), interleukin-8 (IL-8), and monocyte chemotactic protein-1 (MCP-1) levels were examined at gene expression and protein level by real-time PCR and ELISA, respectively. AEA and 2-AG did not reveal any significant effects on proliferation/viability of hPdLCs in the absence of P. gingivalis LPS. However, hPdLCs viability was significantly increased by 10–20 µM AEA in the presence of P. gingivalis LPS (1 µg/ml). In the absence of P. gingivalis LPS, AEA and 2-AG did not exhibit any significant effect on the expression of IL-8 and MCP-1 expression in hPdLCs, whereas IL-6 expression was slightly enhanced by 10 µM 2-AG and not affected by AEA. In P.gingivalis LPS stimulated hPdLCs, 10 µM AEA down-regulated gene-expression and protein production of IL-6, IL-8, and MCP-1. In contrast, 10 µM 2-AG had an opposite effect and induced a significant up-regulation of gene and protein expression of IL-6 and IL-8 (P<0.05) as well as gene-expression of MCP-1 in P. gingivalis LPS stimulated hPdLCs. Our data suggest that AEA appears to have an anti-inflammatory and immune suppressive effect on hPdLCs’ host response to P.gingivalis LPS, whereas 2-AG appears to promote detrimental inflammatory processes. In conclusion, AEA and 2-AG might play an important role in the modulation of periodontal inflammation.

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“…This could potentially be explained if iron overload in TM prevents TRPV1 activation from further modifying TRAP levels -which are directly regulated by iron at the gene transcription level. 48 Indeed, TRAP is an iron phosphatase, thus the presence of iron overload, which is characteristic of patients with TM, may activate TRAP transcription per se. On the other hand, the activation of TRAP protein is associated with proteolytic cleavage in an exposed loop domain due to cathepsin K, 23 which was found to be significantly decreased in resiniferatoxin-treated TM-derived osteoclasts ( Figure 3A).…”

Section: Discussionmentioning

confidence: 99%

Iron overload causes osteoporosis in thalassemia major patients through interaction with transient receptor potential vanilloid type 1 (TRPV1) channels

et al. 2014

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Transient receptor potential vanilloid‐1 regulates osteoprotegerin/RANKL homeostasis in human periodontal ligament cells

Abstract: Our study demonstrates that activation of TRPV1 leads to an increase of the OPG/RANKL ratio in HPDL cells. These findings suggest the novel function of TRPV1 in periodontal tissues, at least, as the regulator of the OPG/RANKL axis.

Cited by 21 publications

References 36 publications

Blocking of TRPV-1 in the parodontium relieves orthodontic pain by inhibiting the expression of TRPV-1 in the trigeminal ganglion during experimental tooth movement in rats

Blocking of TRPV-1 in the parodontium relieves orthodontic pain by inhibiting the expression of TRPV-1 in the trigeminal ganglion during experimental tooth movement in rats

Endocannabinoids and Inflammatory Response in Periodontal Ligament Cells

Iron overload causes osteoporosis in thalassemia major patients through interaction with transient receptor potential vanilloid type 1 (TRPV1) channels

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