Expression Profiles of Inflammation-associated microRNAs in Periapical Lesions and Human Periodontal Ligament Fibroblasts Inflammation

Yue, Junli; Song, Dongzhe; Lu, Wanlu; Lü, Ying; Zhou, Wei; Tan, Xuelian; Zhang, Lan; Huang, Dingming

doi:10.1016/j.joen.2016.08.013

Cited by 32 publications

(29 citation statements)

References 33 publications

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“…It has been demonstrated that the miR key regulators Drosha, Dicer, Drosha cofactor DGRC8, and exportin-5 are significantly downregulated during the inflammatory process in the skin (26), indicating that inflammation induces changes in the level of miR maturation machinery. Moreover, miR has been shown to be associated with inflammation, such as downregulation (miR-29b, miR-106b, miR-125b, and miR-198) in apical periodontitis (75) and upregulation (miR-155 and miR-146a) in patients with rheumatoid arthritis (49). Thus ox-LDL, as a major proinflammatory factor, may regulate miR-125a-5p expression via the inflammatory response, probably partly by influencing the expression of Drosha and Dicer in EC.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-125a-5p alleviates the deleterious effects of ox-LDL on multiple functions of human brain microvessel endothelial cells

Pan

Liao

Liu

et al. 2017

American Journal of Physiology-Cell Physiology

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MicroRNA-125a-5p (miR-125a-5p) could participate in the pathogenesis of vascular diseases. In this study, we investigated the role of miR-125a-5p in oxidized low-density lipoprotein (ox-LDL)-induced functional changes in human brain microvessel endothelial cells (HBMEC). The reactive oxygen species (ROS) production, nitric oxide (NO) generation, senescence, apoptosis, and functions of HBMEC were analyzed. For mechanism study, the epidermal growth factor receptor (EGFR)/extracellular signal-regulated protein kinase (ERK)/p38 mitogen-activated protein kinase (p38 MAPK) pathway and phosphatidylinositol-3-kinase (PI3K)/serine/threonine kinase (Akt)/endothelial nitric oxide synthase (eNOS) pathway were analyzed. Results showed the following: ) Expression of miR-125a-5p was reduced in ox-LDL-treated HBMEC.) Overexpression of miR-125a-5p protected HBMEC from ox-LDL-induced apoptosis, senescence, ROS production, and NO reduction. ) Overexpression of miR-125a-5p increased HBMEC proliferation, migration, and tube formation, while decreasing HBMEC adhesion to leukocytes, as well as counteracting the effects of ox-LDL on those functions.) The levels of EGFR/ERK/p38 MAPK pathway, PI3K/Akt/eNOS pathway, cleaved caspase-3, and adherent molecular ICAM-1 and VCAM-1 were associated with the effects of ox-LDL on these HBMEC functions. In conclusion, miR-125a-5p could counteract the effects of ox-LDL on various HBMEC functions via regulating the EGFR/ERK/p38 MAPK and PI3K/Akt/eNOS pathways and cleaved caspase-3, ICAM-1, and VCAM-1 expression.

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Section: Discussionmentioning

confidence: 99%

MicroRNA-125a-5p alleviates the deleterious effects of ox-LDL on multiple functions of human brain microvessel endothelial cells

Pan

Liao

Liu

et al. 2017

American Journal of Physiology-Cell Physiology

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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%

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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“…It has been reported that miRNAs exert vital roles in a variety of inflammatory diseases, such as acute kidney injury [6], adipose tissue inflammation [7], inflammatory bowel disease [8], periapical lesions and human periodontal ligament fibroblast inflammation [9] and allergy and asthma [10]. In addition, a few studies have focused on the relationship between miRNAs and AP.…”

Section: Introductionmentioning

confidence: 99%

miR-155-5p is Negatively Associated with Acute Pancreatitis and Inversely Regulates Pancreatic Acinar Cell Progression by Targeting Rela and Traf3

Liu¹,

Zou²,

Wang³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Acute pancreatitis contributes to high mortality in pancreatitis patients, and miRNAs play a vital role in the development of acute pancreatitis (AP), however, its precise biological role remains largely elusive. Methods: To clarify the potential mechanisms of miRNAs in AP, we built mouse models of mild acute pancreatitis (MAP) and moderate/ severe acute pancreatitis (SAP). MiRNA microarray analysis and Real-time quantitative PCR (qRT-PCR) were used to analyze the expression of miRNA in MAP/SAP. TargetScan software, dual-luciferase gene reporter assays and Western blotting were used to assess the target genes of miR-155-5p in AP. Results: miR-155-5p was significantly decreased in MAP/SAP mice compared to controls. In pancreatic acinar AR42J cells transfected with miR-155-5p mimic, the expression of Rela and Traf3 notably decreased in both the caerulein- and TLC-S-induced groups compared with the negative control (NC); however, the expression of Rela and Traf3 notably increased after transfection with miR-155-5p inhibitor. Combined analysis using the TargetScan software and dual-luciferase gene reporter assays indicated that Rela and Traf3 were both targeted by miR-155-5p. Meanwhile, the expression of Ptgs2 also decreased after transfection of the AR42J cells with miR-155-5p mimic. The opposite results were found when miR-155-5p inhibitor was transfected into the AR42J cells. In addition, we treated caerulein- and TLC-S-induced AR42J cells with the Rela inhibitor helenalin and found that the expression of Rela, Traf3 and Ptgs2 decreased compared with the NC, while the expression of miR-155-5p did not show any significant difference. Furthermore, we found that miR-155-5p was significantly down-regulated in pancreatitis patients. Conclusion: miR-155-5p inversely regulated AP development through the Rela/Traf3/Ptgs2 signaling pathway.

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Expression Profiles of Inflammation-associated microRNAs in Periapical Lesions and Human Periodontal Ligament Fibroblasts Inflammation

Cited by 32 publications

References 33 publications

MicroRNA-125a-5p alleviates the deleterious effects of ox-LDL on multiple functions of human brain microvessel endothelial cells

MicroRNA-125a-5p alleviates the deleterious effects of ox-LDL on multiple functions of human brain microvessel endothelial cells

Inflammatory profile of chronic apical periodontitis: a literature review

miR-155-5p is Negatively Associated with Acute Pancreatitis and Inversely Regulates Pancreatic Acinar Cell Progression by Targeting Rela and Traf3

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