Effects of miR-223 on expression of IL-1β and IL-6 in human gingival fibroblasts

Matsui, Sari; Ogata, Yorimasa

doi:10.2334/josnusd.58.101

Cited by 32 publications

(23 citation statements)

References 36 publications

(35 reference statements)

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“…We found that IL‐1β, IL‐6, β‐actin and fibronectin genes followed this pattern of response. It is interesting to consider that this effect of IL‐1β on IL‐1β transcription may represent an important mechanism that may amplify the inflammatory response in gingival fibroblasts . Therefore, the ability of the chitosan‐triclosan particles to downregulate this effect represents an interesting response that may collaborate in the modulation of inflammation in connective tissue cells.…”

Section: Discussionmentioning

confidence: 99%

“…It is interesting to consider that this effect of IL-1β on IL-1β transcription may represent an important mechanism that may amplify the inflammatory response in gingival fibroblasts. 29 Therefore, the ability of the chitosan-triclosan particles to downregulate this effect represents an interesting response that may collaborate in the modulation of inflammation in connective tissue cells. A synergistic role has been proposed for IL-1β and IL-6 in gingival connective tissue cells that promotes the enhancement of inflammation in gingival tissues.…”

Section: T a B L E 1 Genes Regulated By Chitosantriclosan Particlesmentioning

confidence: 99%

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Chitosan‐triclosan particles modulate inflammatory signaling in gingival fibroblasts

Pavéz

Tobar

Chacón

et al. 2017

J of Periodontal Research

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Section: Discussionmentioning

confidence: 99%

Section: T a B L E 1 Genes Regulated By Chitosantriclosan Particlesmentioning

confidence: 99%

Chitosan‐triclosan particles modulate inflammatory signaling in gingival fibroblasts

Pavéz

Tobar

Chacón

et al. 2017

J of Periodontal Research

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“…IL6 is known to exert an important effect in the pathogenesis of periodontitis [42]. During the development of CP, multiple biological actions could be mediated by the binding of IL-6 and its receptor (IL-6R), including hematopoiesis, angiogenesis induction, immunocyte activation, and osteoclast differentiation [43].…”

Section: Discussionmentioning

confidence: 99%

Interleukin-6-174G/C Polymorphism Contributes to Periodontitis Susceptibility: An Updated Meta-Analysis of 21 Case-Control Studies

Zhu

Guo

et al. 2016

Disease Markers

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Introduction. Chronic Periodontitis (CP) is suggested to be related to gene variations. Present study aims to quantitatively estimate the association between interleukin-6- (IL-6-) 174G/C polymorphism and CP susceptibility. Materials and Methods. Pubmed, Embase, and Web of Science were searched up to May 2016. The meta-analyses were performed using STATA 12.0. Results. 21 studies were yielded. Significant associations were found under heterozygote comparison and dominant model in studies fulfilling HWE (GC versus GG: OR = 0.690, 95% CI = 0.560–0.849, P = 0.000; CC + GC versus GG: OR = 0.690, 95% CI = 0.568–0.838, P < 0.001); significant associations were found under heterozygote comparison and dominant model in Caucasian studies fulfilling HWE (GC versus GG: OR = 0.752, 95% CI = 0.577–0.980, P = 0.035; CC + GC versus GG: OR = 0.737, 95% CI = 0.576–0.944, P = 0.016); significant associations were found under allele comparison, heterozygote comparison, and dominant model in Brazilian population (C versus G: OR = 0.648, 95% CI = 0.497–0.845, P = 0.001; GC versus GG: OR = 0.621, 95% CI = 0.441–0.876, P = 0.007; CC + GC versus GG: OR = 0.649, 95% CI = 0.470–0.896, P = 0.009). Conclusion. IL-6 174 polymorphism is associated with CP susceptibility. In Brazilian and Caucasian population, IL-6 174 GG genotype plays as a risk factor to CP.

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“…). It has been reported that miR‐223 is significantly overexpressed in diseased compared to healthy gingiva, and it controls the inflammatory response in cultured gingival fibroblasts via inhibitory kappa B kinase α (IKKα) and MAP kinase phosphatase (MKP)‐5 (Matsui & Ogata ). Additionally, Guan et al .…”

Section: Introductionmentioning

confidence: 99%

“…Later, it was found to be expressed in bone, adipose tissue (Chuang et al 2015) and cardiac muscle tissue (Rangrez et al 2011) and to affect cell differentiation, inflammation and cancer (Haneklaus et al 2013). It has been reported that miR-223 is significantly overexpressed in diseased compared to healthy gingiva, and it controls the inflammatory response in cultured gingival fibroblasts via inhibitory kappa B kinase a (IKKa) and MAP kinase phosphatase (MKP)-5 (Matsui & Ogata 2016). Additionally, Guan et al (2015) found that miR-223 can reciprocally regulate the differentiation of adipocytes and osteoblasts through a C/EBPa/miR-223/ FGFR2 feedback loop.…”

mentioning

confidence: 99%

Inflammation‐induced overexpression of microRNA‐223‐3p regulates odontoblastic differentiation of human dental pulp stem cells by targeting SMAD3

Huang

Liu²,

Hou

et al. 2018

Int Endodontic J

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Aim To profile miRNA expression between inflamed and healthy human dental pulp tissues and to investigate how the upregulation of miR‐223‐3p in the inflamed pulp tissue regulates odontoblast differentiation and regeneration. Methodology Microarray analysis was used to identify differences in miRNA expression patterns between healthy and inflamed pulp tissue. The results were validated using quantitative real‐time PCR. To determine the effect of miR‐223‐3p on odontoblast differentiation, miR‐223‐3p was overexpressed in human dental pulp stem cells (DPSCs), which were cultured in mineralizing induction medium (to induce odontoblast differentiation). To identify the target genes of miR‐223‐3p, an SABiosciences Human Osteogenesis PCR Array, combined with bioinformatics, was used. Furthermore, a dual‐luciferase reporter assay and a small interfering RNA (siRNA) experiment were used to confirm the relationship between miR‐223‐3p and its target gene. Statistical analysis was performed using the Student's t‐test or one‐way analysis of variance (anova); P < 0.05 was considered statistically significant. Results Seventy‐nine miRNAs were significantly differentially expressed (fold change >2.0; P < 0.05) between the two tissues. In particular, miR‐223‐3p was markedly upregulated in inflamed dental pulp. Overexpression of miR‐223‐3p in DPSCs significantly increased the protein levels of dentine sialophosphoprotein (DSPP) and dentine matrix protein 1 (DMP‐1) (P < 0.05). However, the SMAD family member 3 (SMAD3) protein level was significantly lower than in control DPSCs (P < 0.05). Bioinformatics and the dual‐luciferase assay reporter assay indicated that Smad3 was a potential target of miR‐223‐3p. Knockdown of Smad3 in DPSCs subjected to mineralization induction resulted in detection of DSPP and DMP‐1 earlier than in control DPSCs, and it increased the protein level of alkaline phosphatase (ALP), thereby promoting odontoblast differentiation. Conclusions miR‐223‐3p is implicated in the regulation of odontoblast differentiation, which may be involved in the process of pulpitis repair.

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Effects of miR-223 on expression of IL-1β and IL-6 in human gingival fibroblasts

Cited by 32 publications

References 36 publications

Chitosan‐triclosan particles modulate inflammatory signaling in gingival fibroblasts

Chitosan‐triclosan particles modulate inflammatory signaling in gingival fibroblasts

Interleukin-6-174G/C Polymorphism Contributes to Periodontitis Susceptibility: An Updated Meta-Analysis of 21 Case-Control Studies

Inflammation‐induced overexpression of microRNA‐223‐3p regulates odontoblastic differentiation of human dental pulp stem cells by targeting SMAD3

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