The role of extracellular matrix metalloproteinase inducer glycosylation in regulating matrix metalloproteinases in periodontitis

Zhang, Z.; Yang, Xueli; Zhang, H.; Liu, X.; Pan, Shaoxia; Li, C.

doi:10.1111/jre.12524

Cited by 21 publications

(16 citation statements)

References 32 publications

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“…LPS stimulation ( P < .01, Figure B). Protein levels of EMMPRIN/MMP‐2, 9 increased significantly, particularly for EMMPRIN and MMP‐9 ( P < .01, Figure E), and consistent with those of a previous study . In addition, qRT‐PCR results showed similar change trend for β‐catenin, EMMPRIN and MMP‐2, 9 mRNA levels as those of WB ( P < .05, Figure C; P < .001, Figure F).…”

Section: Resultssupporting

confidence: 89%

“…LPS did not influence the expression of EMMPRIN, instead, 10 μg/mL Pg . LPS stimuli obviously upregulated EMMPRIN, which was one of the main targets of this study. Hence, we used 10 μg/mL Pg .…”

Section: Resultsmentioning

confidence: 80%

“…To investigate the functions of these 2 routes in periodontitis, we detected related indicators expression in chronic periodontitis and healthy human gingival sections and performed in vitro experiments by using the HIOEC/HGF co‐culture model, which we successfully established previously. This co‐culture model helped to conduct mechanism studies of periodontitis under conditions that simulated the real physiological microenvironment . In our previous study, although HGF individual and HIOEC/HGF co‐culture models appeared the similar change tendency, the co‐culture model indicated a high sensitivity to stimulation and a more significant change towards the same treatment than an individual culture model.…”

Section: Discussionmentioning

confidence: 91%

See 2 more Smart Citations

Interaction between the Wnt/β‐catenin signaling pathway and the EMMPRIN/MMP‐2, 9 route in periodontitis

Liu

Zhang

Pan

et al. 2018

J of Periodontal Research

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Section: Resultssupporting

confidence: 89%

Section: Resultsmentioning

confidence: 80%

Section: Discussionmentioning

confidence: 91%

See 1 more Smart Citation

Interaction between the Wnt/β‐catenin signaling pathway and the EMMPRIN/MMP‐2, 9 route in periodontitis

Liu

Zhang

Pan

et al. 2018

J of Periodontal Research

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“…Overexpression of MMPs is necessary at the early step of tissue destruction to allow the periodontopathic bacterias, immune cells, and inflammatory factors to invade the healthy periodontium (Hannas et al, 2007;Kim et al, 2013;Ma et al, 2003). Our previous results (Yang et al, 2013;Xiang, Li, Dong, Cao, & Liu, 2009;Zhang et al, 2018) also demonstrated MMP-2, MMP-8, and MMP-9 are the prominent metalloproteinase in periodontitis and are responsible for the degradation of collagen I, II, and III in periodontal ECM, and basement membrane collagen IV.…”

Section: Introductionmentioning

confidence: 86%

Interleukin‐25 regulates matrix metalloproteinase‐2 and ‐9 expression in periodontal fibroblast cells through ERK and P38MAPK pathways

Pan

Zhang

et al. 2020

Cell Biology International

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Interleukin-25 (IL-25) has been recognized as a new member of the IL-17 family and implicated in various inflammatory pathology. We aimed to investigate the effects of IL-25 on the expression of matrix metalloproteinase-2 (MMP-2), MMP-8, and MMP-9 in periodontal fibroblast cells (PFCs), cell migration, cytoskeleton F-actin, and to explore the involved extracellular-regulated protein kinases (ERKs), P38 mitogenactivated protein kinase (P38MAPK) signaling pathways, and IL-17 receptor. To evaluate the expression of MMP-2, MMP-8, MMP-9, and F-actin, PFCs were treated by various doses of IL-25 (0, 20, 50, 100, and 500 ng/ml). Protein expression of extracellular metalloproteinase inducer (EMMPRIN) was also evaluated by western blot. Cell scratches experiment was performed to test the cell migration ability. ERK, P38MAPK, and Jun N-terminal kinase signal pathways and related expression of PERK and P-P38MAPK were examined after treatment of different doses of IL-25 and after treatment of inhibitors of ERK and P38MAPK. Immunofluorescence of MMP-2, MMP-9, and F-actin were evaluated after inhibitor treatment. IL-17RB small interfering RNA was used to examine the receptor of IL-25. IL-25 increased the protein expression of MMP-2 and MMP-9. MMP-8 and EMMPRIN expressions were not regulated by IL-25 in PFCs. Positive IF staining extended strongly from the central part to the whole cell. IL-25 mediated MMP-2, MMP-9, F-actin expressions and cell migration were regulated by P38MAPK and ERK pathways, and IL-17RB. SB203580 and U0126 blocked the effects of IL-25 through the inhibition of ERK, P38MAPK, PERK , and P-P38MAPK. The data indicate that IL-25 could regulate cell migration, MMP-2, and MMP-9 expression, but not MMP-8 expression, in PFCs. Moreover, the regulation effects were involved in ERK and P38MAPK pathways, and receptor IL-17RB.

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“…MMPs are a family of Zn 2+ -containing neutral proteolytic enzymes that degrade extracellular matrix (ECM). Human MMPs are classified as collagenases, gelatinases, matrix lysins, membrane-type MMPs and other MMPs (14,15). The direct effects of MMPs in periodontal tissue destruction and degradation are involved in the development of periodontitis.…”

Section: Il-18 Promotes the Secretion Of Matrix Metalloproteinases Inmentioning

confidence: 99%

IL‑18 promotes the secretion of matrix metalloproteinases in human periodontal ligament fibroblasts by activating NF‑κB signaling

et al. 2018

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Chronic periodontitis is the most common periodontal disease and is characterized by progressive degeneration of periodontal tissue. Periodontal-specific pathogens can induce the expression of various inflammatory cytokines in periodontal ligament cells and their secretion into peripheral blood. These inflammatory cytokines have an important role in the occurrence and development of chronic periodontitis. ELISA was used to detect the expression of interleukin-18 (IL-18) protein in the serum and saliva of 30 healthy volunteers and 30 patients with chronic periodontitis. The clinical parameters that were assessed included plaque index, gingival index, periodontal probing depth and attachment loss. The effect of IL-18 on the viability of human periodontal ligament fibroblasts (hPDLFs) was examined using a Cell Counting Kit-8 assay. The effects of IL-18 on mRNA expression and secretion of matrix metalloproteinase (MMP)1, MMP2, MMP3 and MMP9 in hPDLFs were detected by reverse transcription-quantitative polymerase chain reaction and ELISA, respectively. The effect of IL-18 on the phosphorylation of nuclear factor-κB (NF-κB) p65 protein and the protein expression of MMP1, MMP2, MMP3 and MMP9 in hPDLF cells was detected by western blotting. The expression level of IL-18 in the serum of patients with chronic periodontitis was significantly higher than that of healthy volunteers, and the expression level of IL-18 in saliva was positively correlated with the periodontal destruction. However, IL-18 did not have a significant effect on the viability ability of hPDLFs. IL-18 promoted phosphorylation of NF-κB p65 protein in hPDLF, and increased the mRNA expression and protein secretion of MMP1, MMP2, MMP3 and MMP9. These findings indicate that IL-18 promotes the secretion of MMP1, MMP2, MMP3, and MMP9 in hPDLFs by activating the NF-κB signaling pathway, which has a key role in the development of chronic periodontitis. Therefore, targeting IL-18 may be a new research direction for the treatment of chronic periodontal disease.

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The role of extracellular matrix metalloproteinase inducer glycosylation in regulating matrix metalloproteinases in periodontitis

Cited by 21 publications

References 32 publications

Interaction between the Wnt/β‐catenin signaling pathway and the EMMPRIN/MMP‐2, 9 route in periodontitis

Interaction between the Wnt/β‐catenin signaling pathway and the EMMPRIN/MMP‐2, 9 route in periodontitis

Interleukin‐25 regulates matrix metalloproteinase‐2 and ‐9 expression in periodontal fibroblast cells through ERK and P38MAPK pathways

IL‑18 promotes the secretion of matrix metalloproteinases in human periodontal ligament fibroblasts by activating NF‑κB signaling

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