Single nucleotide polymorphisms associated with aggressive periodontitis and severe chronic periodontitis in Japanese

Suzuki, Asami; Ji, Guijin; Numabe, Yukihiro; Muramatsu, Masaaki; Gomi, Kazuhiro; Kanazashi, Mikimoto; Ogata, Yorimasa; Shimizu, Emi; Shibukawa, Yoshihiro; Ito, Akira; Ito, Taichi; Sugaya, Akira; Arai, Takashi; Yamada, Satoru; Deguchi, Shinji; Kamoi, Kazumi

doi:10.1016/j.bbrc.2004.03.126

Cited by 42 publications

(44 citation statements)

References 24 publications

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“…This observation correlates with the finding that EGF-dependent signaling is involved in regulation of numerous biological pathways in the periodontium, including regulation of cell proliferation, migration, and differentiation (7,16,20). Thus, the importance of EGF in periodontal health is highlighted by the fact that a single-nucleotide polymorphism within the EGF gene has been found to be associated with development of severe chronic periodontitis (21).…”

supporting

confidence: 80%

Inactivation of Epidermal Growth Factor by Porphyromonas gingivalis as a Potential Mechanism for Periodontal Tissue Damage

et al. 2013

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f Porphyromonas gingivalis is a Gram-negative bacterium associated with the development of periodontitis. The evolutionary success of this pathogen results directly from the presence of numerous virulence factors, including peptidylarginine deiminase (PPAD), an enzyme that converts arginine to citrulline in proteins and peptides. Such posttranslational modification is thought to affect the function of many different signaling molecules. Taking into account the importance of tissue remodeling and repair mechanisms for periodontal homeostasis, which are orchestrated by ligands of the epidermal growth factor receptor (EGFR), we investigated the ability of PPAD to distort cross talk between the epithelium and the epidermal growth factor (EGF) signaling pathway. We found that EGF preincubation with purified recombinant PPAD, or a wild-type strain of P. gingivalis, but not with a PPAD-deficient isogenic mutant, efficiently hindered the ability of the growth factor to stimulate epidermal cell proliferation and migration. In addition, PPAD abrogated EGFR-EGF interaction-dependent stimulation of expression of suppressor of cytokine signaling 3 and interferon regulatory factor 1. Biochemical analysis clearly showed that the PPAD-exerted effects on EGF activities were solely due to deimination of the C-terminal arginine. Interestingly, citrullination of two internal Arg residues with human endogenous peptidylarginine deiminases did not alter EFG function, arguing that the C-terminal arginine is essential for EGF biological activity. Cumulatively, these data suggest that the PPAD-activity-abrogating EGF function in gingival pockets may at least partially contribute to tissue damage and delayed healing within P. gingivalis-infected periodontia.

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supporting

confidence: 80%

Inactivation of Epidermal Growth Factor by Porphyromonas gingivalis as a Potential Mechanism for Periodontal Tissue Damage

et al. 2013

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“…Although the host's responses to bacterial challenge in periodontal tissues vary depending on the individual immune genetic heritage; so the genetic factors explain the clinical variability in periodontitis. The evidence for a genetic susceptibility to periodontitis comes from twins (1,2) and association studies (3,4). However, the genetic basis has not been clearly defined.…”

Section: Introductionmentioning

confidence: 99%

Association analysis of the IL-1 gene cluster polymorphisms with aggressive and chronic periodontitis in the Algerian population

Boukortt

Saidi-Ouahrani

Boukerzaza³

et al. 2015

Archives of Oral Biology

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“…Patients with periodontal pockets <5 mm have a reduced EGF concentration compared to patients with periodontal pockets >5 mm. Additionally a single nucleotide mutation within the EGF coding sequence was associated with the development of severe chronic periodontitis [11]. Concerning EGFR, its expression seemed to be limited to the gingival epithelium, since a very low level of expression appeared within the periodontal ligament.…”

Section: Introductionmentioning

confidence: 99%

Porphyromonas gingivalis and its lipopolysaccharide differently modulate epidermal growth factor–dependent signaling in human gingival epithelial cells

Elkaïm

Bugueno

Benkirane‐Jessel

et al. 2017

Journal of Oral Microbiology

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Periodontitis is an inflammatory disease induced by pathogenic bacteria such as Porphyromonas gingivalis. Little is known about epidermal growth factor (EGF) signals in human gingival epithelial cells (HGEC), which are major targets of P. gingivalis, and how the expression of proteins participating in EGF signaling—that is, EGF-receptor (EGFR), suppressor of cytokine signaling-3 (SOCS-3), interferon regulatory factor-1 (IRF-1), and signal transducers and activators of transcription (STAT-3)—are modified. This study aimed to assess the effects of P. gingivalis and its purified lipopolysaccharide (LPS-Pg) on EGF signaling. HGEC were infected for 2 h in a dose-dependent manner with P. gingivalis and with heat-killed P. gingivalis, and activated for 2 and 24 h by 1 µg/mL of purified LPS-Pg. Quantitative reverse transcription polymerase chain reaction and Western blotting were performed to measure mRNA and protein levels for SOCS-3, IRF-1 EGF, EGFR, and STAT-3. The tyrosine-phosphorylation status of STAT-3 was also examined. The results showed that infection of HGEC cells with P. gingivalis, but not with heat-killed P. gingivalis, led to significant reductions in expression levels of mRNAs and proteins for SOCS-3, IRF-1, and EGFR, while LPS-Pg over time significantly increased the expression of these mRNAs and proteins. Tyrosine-phosphorylation of STAT-3 was significantly increased during infection with P. gingivalis and activation by LPS-Pg but not modified during infection with heat-killed P. gingivalis. This study highlights that P. gingivalis and its purified LPS differentially modulated the expression of proteins (SOCS-3, IRF-1, EGFR, and STAT-3) interfering with EGF signaling.

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Single nucleotide polymorphisms associated with aggressive periodontitis and severe chronic periodontitis in Japanese

Cited by 42 publications

References 24 publications

Inactivation of Epidermal Growth Factor by Porphyromonas gingivalis as a Potential Mechanism for Periodontal Tissue Damage

Inactivation of Epidermal Growth Factor by Porphyromonas gingivalis as a Potential Mechanism for Periodontal Tissue Damage

Association analysis of the IL-1 gene cluster polymorphisms with aggressive and chronic periodontitis in the Algerian population

Porphyromonas gingivalis and its lipopolysaccharide differently modulate epidermal growth factor–dependent signaling in human gingival epithelial cells

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