MicroRNA Modulation in Obesity and Periodontitis

Perri, Romina; Nares, Salvador; S., Zhang,; Barros, Silvana P.; Offenbacher, Steven

doi:10.1177/0022034511425045

Cited by 126 publications

(145 citation statements)

References 26 publications

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“…The results suggest that these networks, diseases, and biofunctions regulate the cell cycle and cellular movement of inflammatory and immune cells in gingival tissues. The expressions of specific miRNAs in inflamed gingival tissue and obesity may share inflammatory metabolic mRNA targets (13). These findings offer insight regarding the mechanisms of periodontal inflammation.…”

Section: Discussionmentioning

confidence: 87%

“…56, No. 4,[253][254][255][256][257][258][259][260]2014 Original MicroRNA expression in inflamed and noninflamed gingival tissues from Japanese patients several miRNAs that share inflammatory and metabolic mRNA targets (13). For example, miRNA-146 inhibits proinflammatory cytokine secretion through IL-1 receptor-associated kinase 1 in human gingival fibroblasts (14).…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA expression in inflamed and noninflamed gingival tissues from Japanese patients

et al. 2014

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Periodontitis is a chronic inflammatory disease caused by specific bacteria and viruses. Local, systemic, and environmental factors affect the rate of disease progression. Immune responses to bacterial products, and the subsequent production of inflammatory cytokines, are crucial in the destruction of periodontal tissue. MicroRNAs (miRNAs) are a class of small RNAs that control various cell processes by negatively regulating protein-coding genes. In this study, we compared miRNA expression in inflamed and noninflamed gingival tissues from Japanese dental patients. Total RNAs were isolated from inflamed and noninflamed gingival tissues. miRNA expression profiles were examined by an miRNA microarray, and the data were analyzed by GeneSpring GX, Ingenuity Pathways Analysis, and the TargetScan databases. Observed miRNA expression levels in inflamed gingiva were confirmed by real-time PCR. The three most overexpressed (by >2.72-fold) miRNAs were hsa-miR-150, hsa-miR-223, and hsa-miR-200b, and the three most underexpressed (by <0.39-fold) miRNAs were hsa-miR-379, hsa-miR-199a-5p, and hsa-miR-214. In IPA analysis, hsa-miR-150, hsa-miR-223, and hsa-miR-200b were associated with inflammatory disease, organismal injury, abnormalities, urological disease, and cancer.

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Section: Discussionmentioning

confidence: 87%

Section: Introductionmentioning

confidence: 99%

MicroRNA expression in inflamed and noninflamed gingival tissues from Japanese patients

et al. 2014

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“…A comprehensive screening of periodontitisaffected gingiva (Stoecklin-Wasmer et al 2012) identified a specific miRNA profile and examined the mRNA expression of predicted targets in a transcriptomic dataset. Obese individuals were included only in 1 of these profiling studies, which used a selective miRNA array and a limited number of obese individuals (n = 5) with periodontitis (Perri et al 2012). miRNAs regulate gene expression by providing negative feedback in a broad array of cellular processes that occur in periodontitis and that may be affected by obesity.…”

Section: Introductionmentioning

confidence: 99%

Upregulation of Gingival Tissue miR-200b in Obese Periodontitis Subjects

et al. 2015

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“…org). Finally, miR-22 is fully conserved between human and mouse and has been reported to be involved in cardiovascular diseases and metabolic regulation [25][26][27] . Although PP2Cm performs crucial roles in cells, little is known about the regulatory mechanism of PPM1K gene expression.…”

Section: Introductionmentioning

confidence: 99%

Regulation of PP2Cm expression by miRNA-204/211 and miRNA-22 in mouse and human cells

et al. 2015

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Aim:The mitochondrial targeted 2C-type serine/threonine protein phosphatase (PP2Cm) is encoded by the gene PPM1K and is highly conserved among vertebrates. PP2Cm plays a critical role in branched-chain amino acid catabolism and regulates cell survival. Its expression is dynamically regulated by the nutrient environment and pathological stresses. However, little is known about the molecular mechanism underlying the regulation of PPM1K gene expression. In this study, we aimed to reveal how PPM1K expression is affected by miRNA-mediated post-transcriptional regulation. Methods: Computational analysis based on conserved miRNA binding motifs was applied to predict the candidate miRNAs that potentially affect PPM1K expression. Dual-luciferase reporter assay was performed to verify the miRNAs' binding sites in the PPM1K gene and their influence on PPM1K 3'UTR activity. We further over-expressed the mimics of these miRNAs in human and mouse cells to examine whether miRNAs affected the mRNA level of PPM1K. Results: Computational analysis identified numerous miRNAs potentially targeting PPM1K. Luciferase reporter assays demonstrated that the 3'UTR of PPM1K gene contained the recognition sites of miR-204 and miR-211. Overexpression of these miRNAs in human and mouse cells diminished the 3'UTR activity and the endogenous mRNA level of PPM1K. However, the miR-22 binding site was found only in human and not mouse PPM1K 3'UTR. Accordingly, PPM1K 3'UTR activity was suppressed by miR-22 overexpression in human but not mouse cells. Conclusion: These data suggest that different miRNAs contribute to the regulation of PP2Cm expression in a species-specific manner. miR-204 and miR-211 are efficient in both mouse and human cells, while miR-22 regulates PP2Cm expression only in human cells.

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MicroRNA Modulation in Obesity and Periodontitis

Abstract: A supplemental appendix to this article is published electronically only at http://jdr.sagepub.com/supplemental.

Cited by 126 publications

References 26 publications

MicroRNA expression in inflamed and noninflamed gingival tissues from Japanese patients

MicroRNA expression in inflamed and noninflamed gingival tissues from Japanese patients

Upregulation of Gingival Tissue miR-200b in Obese Periodontitis Subjects

Regulation of PP2Cm expression by miRNA-204/211 and miRNA-22 in mouse and human cells

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