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

Leite, Fábio Renato Manzolli; Aquino, Sabrina García de; Guimarães, Morgana Rodrigues; Cirelli, Joni Augusto; Rossa, Carlos

doi:10.7243/2053-213x-2-1

Cited by 9 publications

(7 citation statements)

References 28 publications

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“…Because these diseases present a cyclic evolution, the immunoinflammatory events responsible for tissue breakdown may not always be active in cross‐sectional studies with a single moment of fluid collection. Additionally, although it is documented that cytokines result from active overlapping intracellular signaling pathways, 2,5,6 many studies described only two or three cytokines, making it impossible to establish relations among them.…”

Section: Discussionmentioning

confidence: 99%

“…3,4 Periodontal tissue inflammation via the biofilm starts with a cellular activation through an interaction between bacterial endotoxins (e.g., lipopolysaccharides) and cell receptors (e.g., tolllike receptor-4) and nucleotide-binding oligomerization domain receptors (NODlike receptors). 5,6 A complex activation of multiple intracellular signaling pathways is initiated with subsequent phosphorylation culminating in nuclear transcription of proinflammatory messengers. 7 The cytokine network, activated in diseased periimplant tissue, is complex because of the overlapping role of many cytokines and is subject to shifts depending on disease activity.…”

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confidence: 99%

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Can Peri‐Implant Crevicular Fluid Assist in the Diagnosis of Peri‐Implantitis? A Systematic Review and Meta‐Analysis

Faot

Nascimento

Campão

et al. 2015

Journal of Periodontology

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Can Peri‐Implant Crevicular Fluid Assist in the Diagnosis of Peri‐Implantitis? A Systematic Review and Meta‐Analysis

Faot

Nascimento

Campão

et al. 2015

Journal of Periodontology

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“…As shown in Figure 7 J, JNK knockdown blocked LPS-induced upregulation of Siglec-E expression and Syk knockdown restored LTA-induced downregulation of Siglec-E expression in Raw264.7 cells. RANKL and TRAF6 are regulators of L. monocytogenes infection via the TLR2 pathway, and upregulated RANKL and TRAF6 reduce phosphorylation of Syk ( Leite, 2014 ; Konno et al., 2009 ; Knoop et al., 2009 ). Real-time PCR revealed the expression of RANKL and TRAF6 was significantly increased after infection with L. monocytogenes on neutrophils isolated from mouse bone marrow ( Figures 7 K and 7L).…”

Section: Resultsmentioning

confidence: 99%

Selective Response to Bacterial Infection by Regulating Siglec-E Expression

Yang

Liu

et al. 2020

iScience

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Summary Interactions between microbes and hosts can be a benign, deleterious, or even fatal, resulting in death of the host, the microbe, or both. Sialic acid-binding immunoglobulin-like lectins (Siglecs) suppress infection responses to sialylated pathogens. However, most pathogens are nonsialylated. Here we determined Siglecs respond to nonsialylated Gram-negative bacteria ( Escherichia coli 25922 and DH5α ) and Gram-positive bacteria ( Staphylococcus aureus and Listeria monocytogenes ). We found that Siglece −/− mice had higher mortality than wild-type mice following Gram-negative but not Gram-positive bacterial infection. Better survival in wild-type mice depended on more efficient clearance of Gram-negative than Gram-positive bacteria. Gram-negative bacteria upregulated Siglec-E, thus increasing reactive oxygen species (ROS); Tyr432 in the ITIM domain of Siglec-E was required to increase ROS. Moreover, Gram-negative bacteria upregulated Siglec-E via TLR4/MyD88/JNK/NF-κB/AP-1, whereas Gram-positive bacteria downregulated Siglec-E via TLR2/RANKL/TRAF6/Syk. Thus, our study describes a fundamentally new role for Siglec-E during infection.

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“…These proinflammatory cytokines stimulate osteoclast differentiation and activity through the modulation of the RANKL/RANK/OPG pathway [6,7]. Increased RANKL:OPG ratios determine osteoclastogenesis and bone resorption through the nuclear factor κB and protein kinase B-mediated signaling pathways [6,7]; whereas reduced RANK-L:OPG ratios favor bone formation. In our study, the RANKL:OPG ratio was increased in the weight gain group and as a result, bone repair was delayed.…”

Section: Discussionmentioning

confidence: 99%

“…Additionally, as a consequence of the expansion of the adipose tissue during weight gain, macrophages infiltrate the tissue, increasing the inflammatory load [5]. IL-1, IL-6 and IL-8 can indirectly modulate the expression of the receptor activator of NF-kappa B ligand (RANKL) and osteoprotegerin (OPG) which may ultimately result in bone loss [6,7].…”

Section: Introductionmentioning

confidence: 99%

Influence of weight gain on the modulation of wound healing following tooth extraction

Furuse

Almeida

Costa

et al. 2018

Bone

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Introduction: Obesity is characterized by extreme body fat accumulation related to lean body mass. The low-grade systemic inflammation induced by weight gain may influence wound healing. This study assessed the association between obesity and alveoli repair after tooth extraction. Methods: Forty-two male Wistar rats were randomly divided into two groups: weight gain (n = 21), animals fed with hyperlipidic cafeteria diet in order to gain weight; and control (non-obese; n = 21) regularly fed rats. After twelve weeks, the upper right central incisor was extracted and animals were sacrificed after 7, 14 and 28 days. Slides were obtained for histological analysis. Bone formation and protein expression at the different periods were compared using Kruskal-Wallis test and Dunn post-test. Results: Bone area was higher in the control group all over the experiment with more TRAP-positive cells and TRAP-positive labeling in the weight gain group. RANKL was homogeneously expressed along the experiment with no differences among the groups; conversely OPG levels reduced in the weight gain groups 14 and 28 days after tooth extraction. Osteocalcin labeling was higher in the control group after 7 days of extraction, with no differences at later time points. VEGF labeling was higher in the control group after 14 days of tooth extraction while the strongest immunolabeling in the weight gain group was observed 21 days post-extraction. Conclusion: Weight gain induced a delay in bone repair after tooth extraction. The increase in the number of TRAP-positive cells observed in the extraction site seems to be mediated by the reduction in the expression of OPG rather than an overexpression of RANKL. In addition, the late expression of VEGF in the weight gain group might have delayed osteoblast migration and differentiation.

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

Cited by 9 publications

References 28 publications

Can Peri‐Implant Crevicular Fluid Assist in the Diagnosis of Peri‐Implantitis? A Systematic Review and Meta‐Analysis

Can Peri‐Implant Crevicular Fluid Assist in the Diagnosis of Peri‐Implantitis? A Systematic Review and Meta‐Analysis

Selective Response to Bacterial Infection by Regulating Siglec-E Expression

Influence of weight gain on the modulation of wound healing following tooth extraction

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