LOX-1 is involved in TLR2 induced RANKL regulation in peri-implantitis

Zhang, Qian; Liu, Jie; Ma, Lei; Bai, Na; Xu, Huilin

doi:10.1016/j.intimp.2019.105956

Cited by 7 publications

(3 citation statements)

References 40 publications

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“…Inspired by the findings in previous studies (Huang et al 2018;Zhang et al 2019), we propose that a combination of TLR2 agonists and miR-146a mimics may have a better response to OVA-induced allergic asthma. Experiments in vivo in our study have also proved that the combination of these two can achieve better therapeutic effect than using one alone.…”

Section: Discussionmentioning

confidence: 77%

Combination of TLR agonist and miR146a mimics attenuates ovalbumin-induced asthma

Wang

et al. 2020

Mol Med

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Background microRNA-146a has been reported to be a regulator in the process of attenuating asthma by inhibiting Toll-like receptor 2 (TLR2) pathway. This study aimed to investigate how miR146a-inhibitor affect the symptom of asthma and the underlying mechanisms. Methods Ovalbumin (OVA)-induced allergic asthma mice model was established by intraperitoneal injection with 20 μg of OVA. Total cells and differential inflammatory cells in bronchoalveolar lavage fluid were counted by flow cytometry. The expression levels of molecules and cytokines in TLR2 signaling pathway were detected by Q-PCR and ELISA. Results miR146a-inhibitor attenuated OVA-induced allergic asthma by increasing Th1 cytokines in OVA-induced allergic asthma model, and the treatment of miR146a-inhibitor can reduce the inflammation caused by asthma, followed by the down-regulation of IL-5 and IL-13 in sorted ILC2. The inhibition of miR-146a significantly reduced symptoms of asthma model with TLR2-related molecules being up-regulated. Conclusion It was found that miR-146a is an important regulator in OVA-induced allergic asthma model, which can relieve symptoms of asthma through regulating TLR2 pathway. These findings provide a theoretical basis for solving asthma in clinical treatment.

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Section: Discussionmentioning

confidence: 77%

Combination of TLR agonist and miR146a mimics attenuates ovalbumin-induced asthma

Wang

et al. 2020

Mol Med

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“…Meanwhile, other PRR-related pathways should also be investigated in further study. For example, the TLR2 pathway has been confirmed both in the pathogenesis of periodontitis and peri-implantitis ( 56 , 57 ); LPS and TLR4 pathway has been widely studied for the regulation in periodontitis and peri-implantitis ( 43 , 56 ); and also other PRRs pathways should be considered ( 47 , 48 ). Similarly, multiple cells, such as natural killer cells, mast cells, and neutrophils, should also be studied in the future as they are involved in innate immune responses ( 58 ).…”

Section: Discussion and Perspectivesmentioning

confidence: 99%

The potential role of cfDNA-related innate immune responses in postoperative bone loss after alveolar bone grafting

2023

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The purpose of treating alveolar bone cleft is to restore a normal maxilla structure. Multiple factors have been identified that can affect the success of alveolar bone grafting. However, with consistent treatment modifications, the surgical outcomes have been improved, but alveolar bone loss still exists. Thus, a new aspect should be found to solve this problem. As alveolar bone belongs to the periodontal tissues, the mechanism of the alveolar bone loss after bone grafting in patients with alveolar bone cleft may be similar to the development of alveolar bone loss in periodontitis. Cell-free DNA (cfDNA) has been demonstrated as a key promoter of alveolar bone loss during periodontal inflammation. We hypothesized that cfDNA-related innate immune responses could be a major inducement for postoperative bone loss after alveolar bone grafting. In this perspective, we preliminarily proved the potential association between cfDNA, TLR9 pathway, and alveolar bone grafting operation, and it might verify that surgical trauma could accumulate cfDNA, which can further activate cellular TLR9 signaling.

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“…Peri-implantitis is the development of serious inflammatory lesions following dental implant therapy. The surrounding hard and soft tissues are affected in peri-implantitis, which can lead to the loss of the implant (2). Previous studies of these therapeutic strategies have not been able to identify a single treatment regimen that is suitably effective against peri-implantitis (3-5).…”

Section: Introductionmentioning

confidence: 99%

Lectin‑type oxidized LDL receptor 1 modulates matrix metalloproteinase 2 production in peri‑implantitis

Zhang

Bai

et al. 2021

Exp Ther Med

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Peri-implantitis is a disease in which inflammatory lesions that affect the surrounding soft and hard tissues develop. Matrix metalloproteinase 2 (MMP2) is hypothesized to be involved in this destructive process. However, the regulatory mechanism of action of MMP2 in the peripheral tissues of the implant are not fully understood. To determine the expression of MMP2 in peri-implantitis, peri-implant crevicular fluid (PICF) was collected from patients with peri-implantitis. The healthy volunteers' peripheral blood human macrophages infected with Porphyromonas gingivalis (P. gingivalis) were used as a cell model to explore the regulatory mechanism of MMP2 regarding dental implants. Western blotting, reverse transcriptionquantitative PCR and immunofluorescence staining were used to measure the expression of MMP2 in the present study. MMP2 expression was increased in the PICF of the patients with peri-implantitis and in human macrophages infected with P. gingivalis. Lectin-type oxidized LDL receptor 1 (LOX-1) mediated the expression of MMP2 in human macrophages upon infection of P. gingivalis, whereas dendritic cell-associated c-type lectin-1 did not appear to be involved in this regulatory process. However, JNK and ERK1/2 were involved in P. gingivalis induced MMP2 expression. The results of this study showed that MMP2 was involved in peri-implantitis. MMP2 was upregulated by LOX-1 in a JNK and ERKk1/2 signaling dependent manner in the cell model. The LOX-1/MMP2 signaling pathway may thus be a potential target for management of peri-implantitis.

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LOX-1 is involved in TLR2 induced RANKL regulation in peri-implantitis

Cited by 7 publications

References 40 publications

Combination of TLR agonist and miR146a mimics attenuates ovalbumin-induced asthma

Combination of TLR agonist and miR146a mimics attenuates ovalbumin-induced asthma

The potential role of cfDNA-related innate immune responses in postoperative bone loss after alveolar bone grafting

Lectin‑type oxidized LDL receptor 1 modulates matrix metalloproteinase 2 production in peri‑implantitis

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