MicroRNA-335-5p Plays Dual Roles in Periapical Lesions by Complex Regulation Pathways

Yue, Junli; Wang, Puyu; Hong, Qiaonan; Liu, Qian; Li, Yan; Xu, Wei; Chen, Xi; Zheng, Qianqian; Zhang, Lan; Huang, Dingming

doi:10.1016/j.joen.2017.03.018

Cited by 23 publications

(20 citation statements)

References 33 publications

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“…Micro-RNAs (miRNAs) are small non-coding RNAs accounting for the regulation of gene expression at the post-transcriptional level [78][79][80]. They act as controllers of several biological activities, including differentiation, proliferation and apoptosis [78].…”

Section: Other Inflammatory Markersmentioning

confidence: 99%

“…They act as controllers of several biological activities, including differentiation, proliferation and apoptosis [78]. Changes in the miRNA expression affect the expression of its target-genes, thus influencing various cell signalling pathways [79]. The profile of miRNA expression can be considered as a diagnostic and prognostic marker in a number of conditions, including odontogenic tumours [81].…”

Section: Other Inflammatory Markersmentioning

confidence: 99%

“…Yue et al [79] assessed the expression of miRNAs (miR-29b, 106b, 125b, 143, 155 and 198) associated with inflammation involving AP lesions and human periodontal ligament fibroblasts (HPDLFs), showing that all of them were significantly up-regulated in tissues of asymptomatic AP. On the other hand, miR-29b, 106b, 125b and 198 were significantly reduced in acute inflammation involving HPDLFs, whereas miR-143 and 155 suffered no change, thus suggesting that miRNA expressions associated with inflammation were different between AP lesions and HPDLFs.…”

Section: Other Inflammatory Markersmentioning

confidence: 99%

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Inflammatory profile of chronic apical periodontitis: a literature review

Braz‐Silva

Bergamini

Mardegan

et al. 2018

Acta Odontologica Scandinavica

160

129

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Apical periodontitis caused by root canal infection is the most frequent pathological lesion in the jaws, mainly manifested as periapical granulomas and cysts. Understanding of the formation and progression of apical periodontitis as well as the identification of inflammatory biomarkers can help increase the knowledge of pathogenic mechanisms, improve the diagnosis and provide support for different therapeutic strategies. The objective of the present article is to review inflammatory biomarkers such as cytokines, chemokines, inflammatory cells, neuropeptides, RANK/RANKL/OPG system and other inflammatory markers and to relate these systems to the development and progression of pathological conditions related to apical periodontitis.

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Section: Other Inflammatory Markersmentioning

confidence: 99%

Section: Other Inflammatory Markersmentioning

confidence: 99%

Section: Other Inflammatory Markersmentioning

confidence: 99%

See 1 more Smart Citation

Inflammatory profile of chronic apical periodontitis: a literature review

Braz‐Silva

Bergamini

Mardegan

et al. 2018

Acta Odontologica Scandinavica

160

129

View full text Add to dashboard Cite

show abstract

“…This microRNA targets semaphorin 3a, known to play a role in bone remodeling and macrophage apoptosis. Another microRNA reported to have a potential role in the pathogenesis of AP is miR-335-5p, a promoter of RANKL (Yue et al, 2017).…”

Section: The Role Of Micrornas In Regulating Pulpal and Periapical DImentioning

confidence: 99%

Genetic and Epigenetic Characterization of Pulpal and Periapical Inflammation

et al. 2020

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Pulpal and periapical diseases affect a large segment of the population. The role of microbial infections and host effector molecules in these diseases is well established. However, the interaction between host genes and environmental factors in disease susceptibility and progression is less well understood. Studies of genetic polymorphisms in disease relevant genes have suggested that individual predisposition may contribute to susceptibility to pulpal and periapical diseases. Other studies have explored the contribution of epigenetic mechanisms to these diseases. Ongoing research expands the spectrum of non-coding RNAs in pulpal disease to include viral microRNAs as well. This review summarizes recent advances in the genetic and epigenetic characterization of pulpal and periapical disease, with special emphasis on recent data that address the pathogenesis of irreversible pulpal pathosis and apical periodontitis. Specifically, proinflammatory and anti-inflammatory gene expression and gene polymorphism, as well as recent data on DNA methylation and microRNAs are reviewed. Improved understanding of these mechanisms may aid in disease prevention as well as in improved treatment outcomes.

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“…67 It is deregulated in rheumatoid arthritis 68 and in periodontal tissue, promoting inflammation via the NF-κB RANKL pathway. 69 mir-335-5p is also a key regulator of canonical Wnt signaling in mesenchymal stem cells, which is integral to connective tissue and bone regulation. 70 Hsa-mir-17-5p is linked to autoimmune disease, and is upregulated in multiple sclerosis affected T-helper cells.…”

Section: Rel Gene Is a Proto-oncogene Associated With B-cell T-cell mentioning

confidence: 99%

Biological links in periodontitis and rheumatoid arthritis: Discovery via text‐mining PubMed abstracts

Acharya

Liu

et al. 2018

J of Periodontal Research

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Background and Objective Primary research concerning molecular pathways that link rheumatoid arthritis with periodontitis is limited. Biomedical literature data mining can offer insights into putative linkage mechanisms toward hypothesis development, based on information discovery. The aim of this study was to explore potential Periodontitis‐Rheumatoid Arthritis biological links by analysing “overlapping” genes reported in biomedical abstracts. Material and Methods PubMed abstracts for terms: (a) “Periodontitis” or “Periodontal Diseases” (PD), (b) “Rheumatoid arthritis” (RA), and (c) their combination with “AND” (RA+PD), were each text‐mined to extract genes using “Human Genome Nomenclature Committee” (HGNC) symbols. A gene‐set common to RA and PD abstracts was determined (RA∩PD). Gene ontology (GO) profiles of RA∩PD and RA+PD were compared using “GoProfiler.” Minimum order protein‐protein interaction (PPI) and gene‐miRNA networks of “differential genes” between RA∩PD and RA+PD were constructed with “networkAnalyst.” Results Among 1676 genes documented in RA (10 5241 abstracts), and 893 genes in PD (80 982 abstracts), 535 genes were common (RA∩PD), from which 35 genes were also documented in RA+PD (415 abstracts). 41 GO‐terms significantly different between RA∩PD and RA+PD GO profiles represented 38 biological processes including; nitric oxide metabolism, immunoglobulin production, hormonal regulation, catabolic process down‐regulation, and leukocyte proliferation. The 500 differential genes’ PPI and gene‐miRNA networks showed REL, TRAF2, AQP1 genes, and miRNAs 335‐5p, 17‐5p, 93‐5p with genes HMOX1 and SP1 as hub nodes. Conclusions Text‐mining biomedical abstracts revealed potentially shared but un‐investigated links between PD and RA, meriting further research.

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MicroRNA-335-5p Plays Dual Roles in Periapical Lesions by Complex Regulation Pathways

Cited by 23 publications

References 33 publications

Inflammatory profile of chronic apical periodontitis: a literature review

Inflammatory profile of chronic apical periodontitis: a literature review

Genetic and Epigenetic Characterization of Pulpal and Periapical Inflammation

Biological links in periodontitis and rheumatoid arthritis: Discovery via text‐mining PubMed abstracts

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