Elevated MicroRNA‐128 in Periodontitis Mitigates Tumor Necrosis Factor‐α Response via p38 Signaling Pathway in Macrophages

Na, Hee Sam; Park, Mi Hee; Song, Yu Ri; Kim, Seyeon; Kim, Hyung‐Joon; Lee, Ju Youn; Choi, Jaeho; Chung, Jin

doi:10.1902/jop.2016.160033

Cited by 28 publications

(30 citation statements)

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“…In the present study, miRNA microarrays were performed to compare the expression of 754 inflammatory‐related miRNAs and no statistical difference was found when CP and AP groups were compared. Current knowledge shows that some studies had examined the expression of miRNAs in inflamed gingival tissues in comparison with healthy gingival tissues (Kalea et al, ; Lee et al, ; Na et al, ; Ogata et al, ; Perri, Nares, Zhang, Barros, & Offenbacher, ; Stoecklin‐Wasmer et al, ; Xie et al, ).…”

Section: Discussionmentioning

confidence: 99%

“…This miRNA is involved in many types of cancer, inflammatory and autoimmune diseases, as well as other pathological processes such as leukaemia, rheumatoid arthritis and cardiovascular disease (Eyholzer et al, ; Sugatani & Hruska, ). Gingival tissues from individuals with periodontitis were also recently investigated, and an increased expression of miR‐128, miR‐34a and miR‐381, and a decreased expression of miR‐15b, miR‐211, miR‐372 and miR‐656 were observed (Na et al, ). Although these previous studies showed many differences between miRNAs expression profiles in healthy and diseased individuals, our investigation observed no difference between AP and CP groups, possibly because groups of diseased subjects were compared.…”

Section: Discussionmentioning

confidence: 99%

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Comparison of miRNA expression profiles in individuals with chronic or aggressive periodontitis

et al. 2018

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Objectives MicroRNAs (miRNAs) may play an important role in inflammatory response. However, the involvement of miRNAs in the pathogenesis of periodontitis is unclear. The present study aimed to compare the miRNA expression profiles in individuals with chronic (CP) or aggressive (AP) periodontitis. Materials and methods Eighteen non‐smoker individuals (CP = 9 and AP = 9) without any history of systemic diseases or previous periodontal therapies were selected at the Clinics of Periodontology from the Federal University of Minas Gerais. Gingival tissue samples were collected during the initial periodontal therapy. miRNAs were isolated, and expression patterns of 754 miRNAs were assessed with a quantitative miRNA PCR array. miRNAs expression profiles were compared between CP and AP groups. Results There were no differences observed in the miRNAs expression profiles between CP and AP (p > 0.05). According to the microarray analyses, the most expressed miRNAs in both groups were hsa‐miR‐1274b, hsa‐let‐7b‐5p, hsa‐miR‐24‐3p, hsa‐miR‐19b‐3p, hsa‐miR‐720, hsa‐miR‐126‐3p, hsa‐miR‐17‐3p and hsa‐miR‐21‐3p. Conclusion Findings suggested no differences in miRNAs expression profiles between chronic and aggressive forms of periodontitis. The overexpression of specific miRNAs could provide insights into the pathogenesis of both forms of the disease.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Comparison of miRNA expression profiles in individuals with chronic or aggressive periodontitis

et al. 2018

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“…Our previous studies demonstrated that miR-146a regulated the cytokine secretion in human gingival fibroblasts and periodontal ligament cells [10, 11]. Recent studies from others delineated that miR-128 controlled the inflammatory response in macrophages after stimulated with porphyromonas gingivalis ( P. gingivalis) [12], and miR-24 acted as a negative regulator in the polarization and plasticity of macrophages activated by P. gingivalis LPS or A. actinomycetemcomitans LPS [13]. …”

Section: Introductionmentioning

confidence: 99%

miR-146a regulates inflammatory cytokine production in Porphyromonas gingivalis lipopolysaccharide-stimulated B cells by targeting IRAK1 but not TRAF6

Jiang

Deng

et al. 2018

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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It has been suggested that microRNAs (miRs) are involved in the immune regulation of periodontitis. However, it is unclear whether and how miRs regulate the function of B cells in the context of periodontitis. This study is to explore the role of miR-146a on the inflammatory cytokine production of B cells challenged by Porphyromonas gingivalis (P. gingivalis) lipopolysaccharide (LPS). Primary B cells were harvested from mouse spleen. Quantitative real-time polymerase chain reaction (qPCR), enzyme-linked immunosorbent assay (ELISA) were used to detect the expression of inflammatory cytokines in B cells in the presence or absence of P. gingivalis LPS and/or miR-146a. Bioinformatics, luciferase reporter assay and overexpression assay were used to explore the binding target of miR-146a. Our results showed that miR-146a level in B cells was elevated by P. gingivalis LPS stimulation, and the mRNA expressions of interleukin (IL)-1β, 6 and 10, and IL-1 receptor associated kinase-1 (IRAK1), but not TNF receptor associated factor 6 (TRAF6), were also upregulated. The expression levels of IL-1β, 6, 10 and IRAK1 were reduced in the presence of miR-146a mimic, but were elevated by the addition of miR-146a inhibitor. MiR-146a could bind with IRAK1 3' untranslated region (UTR) but not TRAF6 3'-UTR. Overexpression of IRAK1 reversed the inhibitory effects of miR-146a on IL-1β, 6 and 10. In summary, miR-146a inhibits inflammatory cytokine production in B cells through directly targeting IRAK1, suggesting a regulatory role of miR-146a in B cell-mediated periodontal inflammation.

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“…To this end, they conducted experiments in which they exposed THP-1 and the oral squamous carcinoma CA9-22 cell lines to P. gingivalis [13]. They subsequently reported increased levels of miR-128 in the THP-1 and the CA9-22 cells [13].…”

Section: Effects Of Mirna-128 On Inflammatory Response In Periodontitismentioning

confidence: 99%

Periodontitis, pathogenesis and progression: miRNA-mediated cellular responses toPorphyromonas gingivalis

Olsen

Singhrao

Osmundsen

2017

Journal of Oral Microbiology

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Porphyromonas gingivalis is considered a keystone pathogen in periodontitis, a disease typically driven by dysbiosis of oral inflammophilic polymicrobial pathobionts. To combat infectious agents, the natural defense response of the host is to switch on inflammatory signaling cascades, whereby microRNA (miRNA) species serve as alternative genetic inhibitory transcriptional endpoints. miRNA profiles from diseased sites differ from those detected in disease-free tissues. miRNA profiles could therefore be harnessed as potential diagnostic/prognostic tools. The regulatory role of some miRNA species (miRNA-128, miRNA-146, miRNA-203, and miRNA-584) in the innate immune system suggests these molecular signatures also have potential in therapy. P. gingivalis–associated miRNAs are likely to influence the innate immune response, whereas its lipopolysaccharide may affect the nature of host miRNAs and their mRNA targets. This mini review discusses miRNA-dependent transcriptional and regulatory phenomena ensuing immune signaling cascade switch-on with development and progression of periodontitis initiated by P. gingivalis exposure.

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Elevated MicroRNA‐128 in Periodontitis Mitigates Tumor Necrosis Factor‐α Response via p38 Signaling Pathway in Macrophages

Abstract: miRNA-128 may be involved in mitigating the inflammatory response induced by P. gingivalis in periodontitis.

Cited by 28 publications

References 50 publications

Comparison of miRNA expression profiles in individuals with chronic or aggressive periodontitis

Comparison of miRNA expression profiles in individuals with chronic or aggressive periodontitis

miR-146a regulates inflammatory cytokine production in Porphyromonas gingivalis lipopolysaccharide-stimulated B cells by targeting IRAK1 but not TRAF6

Periodontitis, pathogenesis and progression: miRNA-mediated cellular responses toPorphyromonas gingivalis

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