Human natural killer cell microRNA: differential expression of MIR181A1B1 and MIR181A2B2 genes encoding identical mature microRNAs

Presnell, Steven R.; Al‐Attar, Ahmad; Cichocki, Frank; Miller, Jeffrey S.

doi:10.1038/gene.2014.65

Cited by 17 publications

(10 citation statements)

References 40 publications

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“…The miR-181 family plays diverse roles in regulating key aspects of cellular growth, development, inflammatory response, differentiation, and autophagy. 24 , 25 , 53 , 54 , 55 , 56 Bioinformatic analysis and our results indicated that miR-181a-5p targets P parα . We found that the intracellular DNA damage and apoptosis induced by overdose WY-14643 treatment were significantly reduced by the ectopic expression of miR-181a-5p.…”

Section: Discussionsupporting

confidence: 53%

Alleviation of Toxicity Caused by Overactivation of Pparα through Pparα-Inducible miR-181a2

Cheng

Wei

Xie

et al. 2017

Molecular Therapy - Nucleic Acids

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Widely varied compounds, including certain plasticizers, hypolipidemic drugs (e.g., ciprofibrate, fenofibrate, WY-14643, and clofibrate), agrochemicals, and environmental pollutants, are peroxisome proliferators (PPs). Appropriate dose of PPs causes a moderate increase in the number and size of peroxisomes and the expression of genes encoding peroxisomal lipid-metabolizing enzymes. However, high-dose PPs cause varied harmful effects. Chronic administration of PPs to mice and rats results in hepatomegaly and ultimately carcinogenesis. Nuclear receptor protein peroxisome proliferator-activated receptor-α (Pparα) was shown to be required for this process. However, biological adaptations to minimize this risk are poorly understood. In this study, we found that miR-181a2 expression was induced by the Pparα agonist WY-14643. Moreover, exogenous expression of miR-181a-5p dramatically alleviated the cell toxicity caused by overactivation of Pparα. Further studies showed that miR-181a-5p directly targeted the Pparα 3′ untranslated region and depressed the Pparα protein level. This study identified a feedback loop between miR-181a-5p and Pparα, which allows biological systems to approach a balance when Pparα is overactivated.

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Section: Discussionsupporting

confidence: 53%

Alleviation of Toxicity Caused by Overactivation of Pparα through Pparα-Inducible miR-181a2

Cheng

Wei

Xie

et al. 2017

Molecular Therapy - Nucleic Acids

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“…3). Recent data show that specific inflammatory cytokines and innate signals, including IL-12/IL-18 or IL-15, and TLR signaling, promote microRNA (miRNA) miR-181a and miR-148a expression in human and murine leukocytes (41, 42) and miR-148a has been shown to directly limit Bach2 expression (43). Altered regulation of Bach2 may function as a mechanistic link by which specific inflammatory cytokines and miRNA regulate T cell differentiation, survival and memory formation.…”

Section: Bach2 Regulation Of Memory T Cell Development and Functionmentioning

confidence: 99%

T Cell Fates Zipped Up: How the Bach2 Basic Leucine Zipper Transcriptional Repressor Directs T Cell Differentiation and Function

Richer

Lang

Butler

2016

The Journal of Immunology

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Recent data illustrate a key role for the transcriptional regulator Bach2 in orchestrating T cell differentiation and function. Although Bach2 has a well-described role in B cell differentiation, emerging data show that Bach2 is a prototypical member of a novel class of transcription factors that regulates transcriptional activity in T cells at super enhancers, or regions of high transcriptional activity. Accumulating data demonstrate specific roles for Bach2 in favoring regulatory T cell generation, restraining effector T cell differentiation and potentiating memory T cell development. Evidence suggests that Bach2 regulates various facets of T cell function by repressing other key transcriptional regulator such as Blimp-1. This review examines our current understanding of the role of Bach2 in T cell function and highlights the growing evidence that this transcriptional repressor functions as a key regulator involved in maintenance of T cell quiescence, T cell subset differentiation and memory T cell generation.

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“…miRNA expression is closely associated with cellular processes such as cell growth, proliferation, and apoptosis. Many studies have investigated the roles of miRNAs in cancer, inflammation, and immunity [ 3 4 5 ]. Recent studies demonstrated that miRNA profiles can be determined from blood [ 6 7 8 ], including circulating miRNAs and those associated with cancer or damaged tissues [ 9 10 ].…”

Section: Introductionmentioning

confidence: 99%

Circulating microRNA expression profiling in young obese Korean women

Choi

Ahn

et al. 2020

Nutr Res Pract

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BACKGROUND/OBJECTIVES This study investigates correlations between circulating microRNAs (miRNAs) and obesity-related parameters among young women (aged 20–30 years old) in Korea. SUBJECTS/METHODS We analyzed TaqMan low density arrays (TLDAs) of circulating miRNAs in 9 lean (body mass index [BMI] < 25 kg/m 2 ) and 15 obese (BMI > 25 kg/m 2 ) women. We also performed gene ontology (GO) analyses of the biological functions of predicted miRNA target genes, and clustered the results using the database for annotation, visualization and integrated discovery. RESULTS The TLDA cards contain 754 human miRNAs; of these, the levels of 8 circulating miRNAs significantly declined (> 2-fold) in obese subjects compared with those in lean subjects, including miR-1227, miR-144-5p, miR-192, miR-320, miR-320b, miR-484, miR-324-3p, and miR-378. Among them, miR-484 and miR-378 displayed the most significant inverse correlations with BMI (miR-484, r = −0.5484, P = 0.0056; miR-378, r = −0.5538, P = 0.0050) and visceral fat content (miR-484, r = −0.6141, P = 0.0014; miR-378, r = −0.6090, P = 0.0017). GO analysis indicated that genes targeted by miR-484 and miR-378 had major roles in carbohydrate and lipid metabolism. CONCLUSION Our result showed the differentially expressed circulating miRNAs in obese subjects compared to lean subjects. Although the mechanistic study to reveal the causal role of miRNAs remains, these miRNAs may be novel biomarkers for obesity.

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Human natural killer cell microRNA: differential expression of MIR181A1B1 and MIR181A2B2 genes encoding identical mature microRNAs

Cited by 17 publications

References 40 publications

Alleviation of Toxicity Caused by Overactivation of Pparα through Pparα-Inducible miR-181a2

Alleviation of Toxicity Caused by Overactivation of Pparα through Pparα-Inducible miR-181a2

T Cell Fates Zipped Up: How the Bach2 Basic Leucine Zipper Transcriptional Repressor Directs T Cell Differentiation and Function

Circulating microRNA expression profiling in young obese Korean women

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