Lipopolysaccharide stimulates expression of osteoprotegerin and receptor activator of NF-kappa B ligand in periodontal ligament fibroblasts through the induction of interleukin-1 beta and tumor necrosis factor-alpha

Wada, Naohisa; Maeda, Hidefumi; Yoshito, Yoshimine; Akamine, Akifumi

doi:10.1016/j.bone.2004.04.023

Cited by 137 publications

(134 citation statements)

References 32 publications

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“…Moreover, TLR4-induced expression of RANKL mRNA in fibroblasts was primarily dependent on p38 MAPK activation. A previous study suggested that RANKL and OPG expression in periodontal ligament cells was indirectly induced by the production of IL-1β and TNF-α 6 hours after LPS stimulation [21]. Our data show that induction of RANKL mRNA occurred mostly 8 hours or more subsequent to stimulation, so we cannot rule out a possible autocrine/paracrine influence by early-response genes in our results.…”

Section: Discussioncontrasting

confidence: 61%

RANKL expression is differentially modulated by TLR2 and TLR4 signaling in fibroblasts and osteoblasts

Leite¹,

Aquino²,

Guimarães³

et al. 2014

Immunol Innov

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Section: Discussioncontrasting

confidence: 61%

RANKL expression is differentially modulated by TLR2 and TLR4 signaling in fibroblasts and osteoblasts

Leite¹,

Aquino²,

Guimarães³

et al. 2014

Immunol Innov

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“…The effects of LPS on OPG and RANKL expression in human periodontal ligament fibroblasts (HPLF) were reported. These suggest that LPS stimulates both OPG and RANKL expression in HPLF by up-regulating IL-1 and TNF- 82 . All of these studies related to the dynamics of the inflammatory process allow a better understanding of the interaction of immunosenescence on cells periodontal.…”

Section: Immunosenescence and Periodontal Cells Interactionmentioning

confidence: 85%

Effects of Human Ageing on Periodontal Tissues

Hebling¹

2012

Periodontal Diseases - A Clinician's Guide

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“…Osteoclasts are present only in bone, where they play a central role in LPS-induced bone loss, such as osteomyelitis, septic arthritis and periodontitis [2,3]. Inhibition of osteoclast function has been considered a protective treatment for inflammatory bone-resorption diseases [15].…”

Section: Discussionmentioning

confidence: 99%

“…Then, inhibition of osteoclast functions and bone resorption is an important approach preventing inflammatory bone-destructive diseases such as osteomyelitis, septic arthritis and periodontitis. Some evidence demonstrates that lipopolysaccharide (LPS), a major component of gram-negative bacterial cell wall, can trigger macrophages and other cells to release a multitude of cytokines, chemokines, metalloproteinases and other agents [2]. Ultimately, these substances activate osteoclasts by receptor activator of nuclear factor kappa-B ligand (RANKL) or macrophage colony-stimulating factor (M-CSF) pathway and induce bone loss [3].…”

Section: Introductionmentioning

confidence: 99%

Bergapten prevents lipopolysaccharide mediated osteoclast formation, bone resorption and osteoclast survival

Zheng

et al. 2013

International Orthopaedics (SICOT)

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Purpose This study was designed to investigate the potential effect of bergapten on lipopolysaccharide (LPS)-mediated osteoclast formation, bone resorption and osteoclast survival in vitro. Methods After osteoclast precursor RAW264.7 cells were treated with bergapten (5, 20, 40 μmol/L) for 72 hours in the presence of LPS (100 ng/ml), osteoclastogenesis was identified by tartrate-resistant acid phosphatase (TRAP) staining, and the number of TRAP-positive multinucleated cells [TRAP(+ )MNCs] per well were counted. To investigate the effect of bergapten on osteoclastic bone resorption, RAW264.7 cells were treated with bergapten for six days in the presence of LPS, and the area of bone resorption was analyzed with Image Pro-Plus. Next, we examined apoptosis of RAW264.7 cells after bergapten incubation for 48 hours by flow cytometer using annexin V/propidium iodide (PI) double labeling. Finally, osteoclast survival was observed by Hoechst 33342 labeling and Western blotting after bergapten treatment for 24 hours. Results Data showed that bergapten (5-40 μmol/L) dosedependently inhibited LPS-induced osteoclast formation and bone resorption. Treatment with bergapten triggered apoptotic death of osteoclast precursor RAW264.7 cells in a dosedependent manner. Furthermore, bergapten significantly reduced the survival of mature osteoclast, as demonstrated by emergence of apoptotic nuclei and activation of apoptotic protein caspase 3/9.Conclusions These findings suggest that bergapten effectively prevents LPS-induced osteoclastogenesis, bone resorption and survival via apoptotic response of osteoclasts and their precursors. The study identifies bergapten as an inhibitor of osteoclast formation and bone resorption and provides evidence that bergapten might be beneficial as an alternative for prevention and treatment of inflammatory bone loss.

show abstract

Lipopolysaccharide stimulates expression of osteoprotegerin and receptor activator of NF-kappa B ligand in periodontal ligament fibroblasts through the induction of interleukin-1 beta and tumor necrosis factor-alpha

Cited by 137 publications

References 32 publications

RANKL expression is differentially modulated by TLR2 and TLR4 signaling in fibroblasts and osteoblasts

RANKL expression is differentially modulated by TLR2 and TLR4 signaling in fibroblasts and osteoblasts

Effects of Human Ageing on Periodontal Tissues

Bergapten prevents lipopolysaccharide mediated osteoclast formation, bone resorption and osteoclast survival

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