Dataset Information

MiR-24, miR-30b, and miR-142-3p regulate phagocytosis in myeloid inflammatory cells.

ABSTRACT: Micro-RNAs (miRNAs) are small noncoding RNAs that regulate various biological pathways. As their role in phagocytosis remains poorly understood, we investigated their impact on phagocytosis in myeloid inflammatory cells. Seven miRNAs (miR-24, -30b, -101, 142-3p, -652-3p, -652-5p, and -1275) that were differentially expressed during monocyte to macrophage (M?) and monocyte to dendritic cell (DC) differentiation were screened for their potential role in phagocytosis. Among these, overexpression of miR-24, miR-30b, and miR-142-3p in human monocyte-derived M?, DC, monocytes, and PBMCs significantly attenuate phagocytosis of Escherichia coli and Staphylococcus aureus, as well as the secretion of inflammatory mediators, including TNF-?, IL-6, and IL-12p40. miRNA-mediated changes in cytokine profiles were observed at transcriptional and/or posttranscriptional levels and importantly exhibit miRNA-specific impact. To examine the underlying mechanism, we monitored the expression of phagocytosis pathway-associated genes and identified several genes that were altered in M? and DC transfected with miR-24, miR-30b, and miR-142-3p mimics. Some of these genes with altered expression also harbor putative miRNA binding sites. We show that miR-142-3p directly regulates protein kinase C? (PKC?), a key gene involved in phagocytosis. Interestingly, miR-142-3p and PKC? exhibit antagonistic expression during M? and DC differentiation. Short interfering RNA-mediated knockdown of PKC? in M? leads to reduced bacterial uptake, further highlighting the role of the gene in phagocytosis. Overall, these results demonstrate that miR-24, miR-30b, and miR-142-3p regulate phagocytosis and associated cytokine production in myeloid inflammatory cells through modulation of various genes involved in the pathway.

SUBMITTER: Naqvi AR

PROVIDER: S-EPMC4323870 | biostudies-literature | 2015 Feb

REPOSITORIES: biostudies-literature

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miR-24, miR-30b, and miR-142-3p regulate phagocytosis in myeloid inflammatory cells.

Naqvi Afsar Raza AR Fordham Jezrom B JB Nares Salvador S

Journal of immunology (Baltimore, Md. : 1950) 20150119 4

Micro-RNAs (miRNAs) are small noncoding RNAs that regulate various biological pathways. As their role in phagocytosis remains poorly understood, we investigated their impact on phagocytosis in myeloid inflammatory cells. Seven miRNAs (miR-24, -30b, -101, 142-3p, -652-3p, -652-5p, and -1275) that were differentially expressed during monocyte to macrophage (Mφ) and monocyte to dendritic cell (DC) differentiation were screened for their potential role in phagocytosis. Among these, overexpression of ...[more]

PMID: 25601927

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Project description:ObjectivePeriodontitis is a chronic inflammatory infectious disease caused by the deposition of dental plaque on the tooth surface, leading to adverse systemic consequences. Accumulating evidence shows that dysregulated microRNAs (miRNAs) are associated with the disease severity of periodontitis. Herein, we report two novel miRNAs, miR-30b-3p and miR-125b-1-3p, in the context of periodontitis and their relationships with disease severity of periodontitis.MethodsThe miRNA profiles of gingival crevicular fluid (GCF) samples were used to screen differentially expressed miRNAs (DEmiRNAs) between periodontitis patients and periodontally healthy individuals. Clinical human GCF samples were collected from 80 patients diagnosed with periodontitis (PD +) for the first time and 100 periodontally healthy individuals (PD-). The severity of periodontitis was categorized into mild/moderate (MPD) and severe (SPD) groups. The expressions of miR-30b-3p and miR-125b-1-3p were determined by quantitative real-time PCR. The levels of IL-1β, IL-6, and TNF-α were determined by ELISA methods.ResultsWe applied GEO2R bioinformatics tool to analyze the raw data of the GSE89081 dataset and identified miR-30b-3p (|logFC|= 1.987) and miR-125b-1-3p (|logFC|= 1.878) between periodontitis patients and periodontally healthy individuals. It was found that PPD, CAL, BOP, and the relative expression levels of miR-30b-3p and miR-125b-1-3p were all higher in the PD + group than the PD- group, in the SPD group than the MPD group (P < 0.05). The periodontitis patients with high-miR-30b-3p expression exhibited increased PPD, CAL, and BOP compared to those low-miR-30b-3p expression, while high-miR-125b-1-3p expression group showed significant differences on PPD and BOP from low-miR-125b-1-3p expression group (P < 0.05). Pearson correlation analysis demonstrated a significantly positive correlation between the levels of inflammatory cytokines, miR-30b-3p expression, and miR-125b-1-3p expression (P < 0.001). Results of ROC curves showed AUC of 0.878 and 0.927, sensitivity of 0.843 and 0.855, and specificity of 0.791 and 0.801, respectively, when miR-30b-3p and miR-125b-1-3p expression levels were used to diagnose periodontitis.ConclusionThese data unveiled that miR-30b-3p and miR-125b-1-3p expressions may be associated with the pathogenesis of periodontitis.

Dataset Information

MiR-24, miR-30b, and miR-142-3p regulate phagocytosis in myeloid inflammatory cells.

Publications

miR-24, miR-30b, and miR-142-3p regulate phagocytosis in myeloid inflammatory cells.

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