Matrix Metalloproteinase‐1 of Gingival Fibroblasts Influenced by Advanced Glycation End Products (AGEs) and Their Association With Receptor for AGEs and Nuclear Factor‐κB in Gingival Connective Tissue

Yu, Shaojie; Li, Huajing; Ma, Ying; Fu, Yao‐Shi

doi:10.1902/jop.2011.100754

Cited by 48 publications

(48 citation statements)

References 40 publications

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“…Meerwaldt reported that skin AF increased statistically in diabetic patients [31]. Furthermore, Yu showed that AGEs upregulate the expression of MMP-1 in HGFs [32]. Similar to the reports, we showed that AGEs induces IL-6 production in HGFs [33].…”

Section: Discussionsupporting

confidence: 89%

High Glucose-Mediated Cytokine Regulation in Gingival Fibroblasts and THP-1 Macrophage: a Possible Mechanism of Severe Periodontitis with Diabetes

Lew

Naruishi

Kajiura

et al. 2018

Cell Physiol Biochem

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Background/Aims: Diabetic patients are susceptible to severe periodontitis, but the precise mechanism is not fully understood. Aim of this study was to explore the biological pathogenesis of severe periodontitis in diabetic patients focusing on the crosstalk of human gingival fibroblasts (HGFs) and macrophages. Methods: A total of 70 periodontitis patients with or without diabetes mellitus (DM) were enrolled, and the statistical relationships of diabetic conditions to the periodontal inflammatory parameters were examined by cross-sectional study. In in vitro study, HGFs cell line CRL-2014® (ATCC) and differentiated THP-1 macrophages were cultured with normal glucose (NG: 5.5 mM) or high glucose (HG: 25 mM) condition, and treated with indicated inflammatory factors such as calprotectin (CPT), interleukin (IL)-1β and IL-6. To examine the effects of HG on soluble IL-6 receptor (sIL-6R) production in THP-1 macrophages, the supernatants were collected and the sIL-6R levels were measured by ELISA. To examine the effects of HG on IL-1β or IL-6-induced matrix metalloproteinase (MMPs) production in HGFs, the supernatants were collected. Levels of MMP-1 and tissue inhibitor of MMP-1 (TIMP-1) were measured by ELISA. Finally, after conditioned medium (CM) from THP-1 macrophages cultured with NG or HG conditions was collected, HGFs were treated with the CM. The supernatants were collected 24 hours later and the levels of MMP-1 and TIMP-1 were measured. To examine the specific effects of IL-1β contained in CM on MMP-1 and TIMP-1 production in HGFs, IL-1 receptor antagonist (IL-1ra) was used. Results: There were statistical correlation between IL-1β and sIL-6R levels in gingival crevicular fluid (GCF) and HbA1c in periodontitis patients with DM (IL-1β: P=0.035, sIL-6R: P=0.040). HG and CPT significantly induced sIL-6R production in THP-1 macrophages. HG significantly enhanced IL-1β or IL-6/sIL-6R-induced MMP-1 production in HGFs. The increase of MMP-1 by both IL-1β and IL-6/sIL-6R was significantly inhibited by specific ERK or IκB inhibitors. Corresponding to the regulation of MMP-1 production, HG condition increased the phosphorylation of p44/42 MAPK and IκBα in HGFs treated with IL-1β or IL-6/sIL-6R. Finally, MMP-1 production in HGFs cultured with HG increased significantly by CM from THP-1 macrophages cultured with HG. The induction of MMP-1 by the CM from THP-1 macrophages cultured with HG was significantly inhibited by dose dependent of IL-1ra in HGFs cultured with HG. Conclusion: Diabetic conditions such as HG induce IL-1β and sIL-6R production from macrophages in inflammatory periodontal tissues and may exacerbate the periodontitis synergistically via MMP-1 production from HGFs.

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Section: Discussionsupporting

confidence: 89%

High Glucose-Mediated Cytokine Regulation in Gingival Fibroblasts and THP-1 Macrophage: a Possible Mechanism of Severe Periodontitis with Diabetes

Lew

Naruishi

Kajiura

et al. 2018

Cell Physiol Biochem

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“…Importantly, the beneficial effects of RAGE blockade were paralleled by suppressed expression of the receptor and its ligands in gingival tissues and were independent of the level of glycaemia. Increased RAGE expression was subsequently reported in other experimental models of diabetes-associated periodontitis (Chang et al 2012a,b, Claudino et al 2012) and in gingival tissues of diabetic individuals with periodontitis, and its expression was correlated to that of NF-kB (Katz et al 2005, Abbass et al 2012, Yu et al 2012. These findings demonstrated that AGE-RAGE interaction may lead to the exaggerated inflammatory response and periodontal tissue destruction seen in diabetes.…”

Section: Hyperglycaemia and Cellular Stressmentioning

confidence: 70%

“…Effects on other relevant cell types have also been reported, such as decreased collagen production and increased collagenolytic activity by gingival and periodontal ligament fibroblasts (Ramamurthy & Golub 1983, Sasaki et al 1992, Yu et al 2012) and a hyper-inflammatory response by oral epithelial cells (Amir et al 2011).…”

Section: Hyperglycaemia and Cellular Stressmentioning

confidence: 98%

A review of the evidence for pathogenic mechanisms that may link periodontitis and diabetes

Taylor

Preshaw

Lalla

2013

Journal of Periodontology

210

258

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A review of the evidence for pathogenic mechanisms that may link periodontitis and diabetes Taylor JJ, Preshaw PM, Lalla E. A review of the evidence for pathogenic mechanisms that may link periodontitis and diabetes.Abstract Aims: To review the evidence for the molecular and cellular processes that may potentially link periodontal disease and diabetes. The pathogenic roles of cytokines and metabolic molecules (e.g. glucose, lipids) are explored and the role of periodontal bacteria is also addressed. Paradigms for bidirectional relationships between periodontitis and diabetes are discussed and opportunities for elaborating these models are considered. Methods: Database searches were performed using MeSH terms, keywords, and title words. Studies were evaluated and summarized in a narrative review. Results: Periodontal microbiota appears unaltered by diabetes and there is little evidence that it may influence glycaemic control. Small-scale clinical studies and experiments in animal models suggest that IL-1b, TNF-a, IL-6, OPG and RANKL may mediate periodontitis in diabetes. The AGE-RAGE axis is likely an important pathway of tissue destruction and impaired repair in diabetesassociated periodontitis. A role for locally activated pro-inflammatory factors in the periodontium, which subsequently impact on diabetes, remains speculative. Conclusion: There is substantial information on potential mechanistic pathways which support a close association between diabetes and periodontitis, but there is a real need for longitudinal clinical studies using larger patient groups, integrated with studies of animal models and cells/tissues in vitro.

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“…It has been reported that RAGEs are found on the surface of smooth muscle cells, endothelial cells, neurons, monocytes, macrophages, and gingival tissues 21‐23 . Hence, far‐ranging effects of activation of the RAGEs can be expected 21‐23 .…”

Section: Discussionmentioning

confidence: 99%

Effect of Glycemic Control on Self‐Perceived Oral Health, Periodontal Parameters, and Alveolar Bone Loss Among Patients With Prediabetes

Javed

AlGhamdi

Mikami

et al. 2014

Journal of Periodontology

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Matrix Metalloproteinase‐1 of Gingival Fibroblasts Influenced by Advanced Glycation End Products (AGEs) and Their Association With Receptor for AGEs and Nuclear Factor‐κB in Gingival Connective Tissue

Abstract: Accumulation of AGEs may upregulate the expression of MMP-1 by HGFs, which may play a role in the development of diabetes-associated periodontitis, and RAGE/NF-κB pathway may be involved in metabolism of MMP-1 in HGFs.

Cited by 48 publications

References 40 publications

High Glucose-Mediated Cytokine Regulation in Gingival Fibroblasts and THP-1 Macrophage: a Possible Mechanism of Severe Periodontitis with Diabetes

High Glucose-Mediated Cytokine Regulation in Gingival Fibroblasts and THP-1 Macrophage: a Possible Mechanism of Severe Periodontitis with Diabetes

A review of the evidence for pathogenic mechanisms that may link periodontitis and diabetes

Effect of Glycemic Control on Self‐Perceived Oral Health, Periodontal Parameters, and Alveolar Bone Loss Among Patients With Prediabetes

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