Toll-like receptor activation and mechanical force stimulation promote the secretion of matrix metalloproteinases 1, 3 and 10 of human periodontal fibroblasts via p38, JNK and NF-kB

Lisboa, Rodolfo Assis; Andrade, Marcus V.; Cunha-Melo, José Renan

doi:10.1016/j.archoralbio.2012.12.009

Cited by 34 publications

(19 citation statements)

References 46 publications

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“…Huja et al reported that bone turnover in the maxilla and mandible of dogs is higher than in the femoral bone, and that bone formation rate in the dog jaw remains high during skeletal maturation, while it decreases with age in femurs (Huja and Beck, 2008; Huja et al, 2006). In addition, mechanical stimulation promotes the secretion of type I collagen and matrix degrading enzymes from human periodontal fibroblasts (Kook et al, 2011; Lisboa et al, 2013), suggesting that mastication contributes to DAMPs production. Taken together, these findings support the idea that jaw tissues are great sources of DAMPs for stimulating the local immune system through TLRs.…”

Section: Discussionmentioning

confidence: 99%

Enhanced TLR-MYD88 Signaling Stimulates Autoinflammation in SH3BP2 Cherubism Mice and Defines the Etiology of Cherubism

et al. 2014

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Summary Cherubism is caused by mutations in SH3BP2. Studies of cherubism mice showed that TNF-α-dependent autoinflammation is a major cause for the disorder, but failed to explain why human cherubism lesions are restricted to jaws and regress after puberty. We demonstrate that the inflammation in cherubism mice is MYD88-dependent and is rescued in the absence of TLR2 and TLR4. However, germ-free cherubism mice also develop inflammation. Mutant macrophages are hyper-responsive to PAMPs (pathogen-associated molecular patterns) and DAMPs (damage-associated molecular patterns) that activate TLRs, resulting in TNF-α overproduction. Phosphorylation of SH3BP2 at Y183 is critical for the TNF-α production. Finally, SYK depletion in macrophages prevents the inflammation. These data suggest that the presence of a large amount of TLR ligands, presumably oral bacteria and DAMPs during jawbone remodeling, may cause the jaw-specific development of human cherubism lesions. Reduced levels of DAMPs after stabilization of jaw remodeling may contribute to the age-dependent regression.

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Section: Discussionmentioning

confidence: 99%

Enhanced TLR-MYD88 Signaling Stimulates Autoinflammation in SH3BP2 Cherubism Mice and Defines the Etiology of Cherubism

et al. 2014

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“…Activation of TLRs has been suggested to modulate the expression levels of certain MMPs but not TIMPs. In a recent study, Lisboa and coworkers showed that activation of TLR-2 and TLR-4, two TLR members expressed by a variety of human cells that participate in the recognition of bacterial lipoproteins and lipopolysaccharides (LPS) [140], induced an increase in the secretion of MMPs-1, -3, and -10 by cultured periodontal fibroblasts, and this was mediated via the p38, JNK1/2, and NF- κ B pathways [141]. It is likely that there is a broad variation in the response of cells to TLR ligands that is dependent on the type of stimulus in the periprosthetic microenvironment.…”

Section: Molecular Mechanisms Controlling the Periprosthetic Micromentioning

confidence: 99%

Extracellular Matrix Degradation and Tissue Remodeling in Periprosthetic Loosening and Osteolysis: Focus on Matrix Metalloproteinases, Their Endogenous Tissue Inhibitors, and the Proteasome

Syggelos

Aletras

Smirlaki

et al. 2013

BioMed Research International

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The leading complication of total joint replacement is periprosthetic osteolysis, which often results in aseptic loosening of the implant, leading to revision surgery. Extracellular matrix degradation and connective tissue remodeling around implants have been considered as major biological events in the periprosthetic loosening. Critical mediators of wear particle-induced inflammatory osteolysis released by periprosthetic synovial cells (mainly macrophages) are inflammatory cytokines, chemokines, and proteolytic enzymes, mainly matrix metalloproteinases (MMPs). Numerous studies reveal a strong interdependence of MMP expression and activity with the molecular mechanisms that control the composition and turnover of periprosthetic matrices. MMPs can either actively modulate or be modulated by the molecular mechanisms that determine the debris-induced remodeling of the periprosthetic microenvironment. In the present study, the molecular mechanisms that control the composition, turnover, and activity of matrix macromolecules within the periprosthetic microenvironment exposed to wear debris are summarized and presented. Special emphasis is given to MMPs and their endogenous tissue inhibitors (TIMPs), as well as to the proteasome pathway, which appears to be an elegant molecular regulator of specific matrix macromolecules (including specific MMPs and TIMPs). Furthermore, strong rationale for potential clinical applications of the described molecular mechanisms to the treatment of periprosthetic loosening and osteolysis is provided.

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“…This change will lead to the degranulation of the mast cells or the change of the morphology and secretory function of the fibroblasts. It shall pass the cascade of stimulating-initiating-information transmitting-amplifying before acting on the target organ [24–26]. In this study, only the role of collagen fibers in this process was observed and there is no observation regarding the morphology or function of the effector cells (the fibroblasts and mast cells, etc.)…”

Section: Discussionmentioning

confidence: 85%

Role of Acupoint Area Collagen Fibers in Anti‐Inflammation of Acupuncture Lifting and Thrusting Manipulation

Fan

Cui

Kuai

et al. 2017

Evidence-Based Complementary and Alternative Medicine

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The role of the acupoint area collagen fibers in the efficacy of acupuncture lifting and thrusting (L&T) manipulation will be explored in this paper. 30 male NZW rabbits were randomly divided into 6 groups: sham operation group (Group N), model group (Group M), acupuncture without manipulation group (Group W), acupuncture L&T manipulation group (Group A), collagenase pretreatment group (Group JM), and collagenase pretreatment + acupuncture L&T manipulation group (Group JA). The bacterial endotoxin was used to generate the rabbit fever models. Acupuncture was applied at IL-11. The levels of IL-1β, TNF-α, and IL-4 and the rectal temperature were measured at 2 h, 4 h, and 6 h after modeling and the collagen fiber morphology at acupoint area was observed after 6 hours. Results. As compared with Group N, the levels of IL-1β and TNF-α in Group M were significantly higher; the level of IL-4 was significantly lower (P < 0.05). As compared with Group M, IL-1β and TNF-α in Groups W and A were significantly lower and IL-4 was significantly higher (P < 0.05). As compared with Group W, IL-1β and TNF-α in Group A were lower and IL-4 was higher (P < 0.05). The collagen fiber in Group A was slightly rough, distorted, and fractured. As shown in studies, the endotoxin-induced inflammatory response can be significantly inhibited by acupuncture whose efficacy can also be significantly improved by the manipulations. Collagenase pretreatment may be the first receptor to the mechanical force of the L&T manipulation.

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Toll-like receptor activation and mechanical force stimulation promote the secretion of matrix metalloproteinases 1, 3 and 10 of human periodontal fibroblasts via p38, JNK and NF-kB

Cited by 34 publications

References 46 publications

Enhanced TLR-MYD88 Signaling Stimulates Autoinflammation in SH3BP2 Cherubism Mice and Defines the Etiology of Cherubism

Enhanced TLR-MYD88 Signaling Stimulates Autoinflammation in SH3BP2 Cherubism Mice and Defines the Etiology of Cherubism

Extracellular Matrix Degradation and Tissue Remodeling in Periprosthetic Loosening and Osteolysis: Focus on Matrix Metalloproteinases, Their Endogenous Tissue Inhibitors, and the Proteasome

Role of Acupoint Area Collagen Fibers in Anti‐Inflammation of Acupuncture Lifting and Thrusting Manipulation

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