MicroRNA-27a/b regulates cellular cholesterol efflux, influx and esterification/hydrolysis in THP-1 macrophages

Zhang, Min; Wu, Jianfeng; Chen, Wujun; Tang, Shilin; Zhang, Mo; Tang, Yue; Li, Yuan; Wang, Jialin; Liu, Xiangyu; Peng, Juan; Chen, Kong; He, Ping; Lv, Yun-Cheng; Ouyang, Xin; Yao, Feng; Tang, Deng-Pei; Cayabyab, Francisco S.; Zhang, Dawei; Zheng, Xi-Long; Tian, Guo-Ping; Tang, Chao-Ke

doi:10.1016/j.atherosclerosis.2014.02.008

Cited by 161 publications

(112 citation statements)

References 50 publications

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“…Our studies have shown that miR-467b targets LPL mRNA in RAW 264.7 macrophages and attenuates lipid accumulation and proinflammatory cytokine secretion, and that, miR476b over-expression protects apoE À/À mice from AS by reducing lipid accumulation and inflammatory cytokine secretion in vivo [75,76]. The miR-27a/b regulate the expression of LPL gene in THP-1 macrophages through binding to its 3 0 UTR, and may play a key role in cholesterol influx and progression of AS [77]. Different miRNA families can share mRNA targets, and a short binding distance between miRNAs may strengthen the repressive effect of multiple miRNAs on one target.…”

Section: Post-transcriptional Regulationmentioning

confidence: 96%

Lipoprotein lipase: From gene to atherosclerosis

Zhang

et al. 2014

Atherosclerosis

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104

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Section: Post-transcriptional Regulationmentioning

confidence: 96%

Lipoprotein lipase: From gene to atherosclerosis

Zhang

et al. 2014

Atherosclerosis

Self Cite

104

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“…Among the 105 miRNA candidates, 14 of them were Ramirez Borel et al, 2012;Kim et al, 2012;Goedeke et al, 2013;Kang et al, 2013;Rottiers et al, 2013;Zhang et al, 2014;Zhao et al, 2014 -298, -354, -7, -200c, -19a/b Kovalchuk et al, 2008;Zhu et al, 2008;Pogribny et al, 2010;Bitarte et al, 2011;Bao et al, 2012;J Chen et al, 2012b -124, -203, -26a, -135b, -145 Furuta et al, 2010;Borel et al, 2012ABCG1 Transporter miR-33 Marquart et al, 2010Rayner et al, 2010 ABCG2/BCRP Transporter miR-520h, -519c, -328, -487a, -181a Liao et al, 2008;Pan et al, 2009b;To et al, 2009;Wang et al, 2010;Li et al, 2011;Padmanabhan et al, 2012;Jiao et al, 2013;Ma et al, 2013SLC6A4 Transporter miR-16, -15a Baudry et al, 2010Tamarapu Parthasarathy et al, 2012;Moya et al, 2013 NR2B1/RXRA Nuclear Receptor miR-27a, -27b Ji et al, 2009;Komagata et al, 2009;Mohri et al, 2009 NR1I1/VD receptor Nuclear Receptor miR-27b, -125b Mohri et al, 2009;Pan et al, 2009aNR1C1 Nuclear Receptor miR-10b, -506, -21, -27b Zheng et al, 2010Kida et al, 2011;Tong et al, 2011;Zhou et al, 2011NR1C3 N...…”

Section: Micrornas Regulate the Expression Of Adme Phase I And Ii Enzmentioning

confidence: 99%

The effects of microRNA on the absorption, distribution, metabolism and excretion of drugs

Chevillet

Liu

et al. 2014

British J Pharmacology

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The importance of genetic factors (e.g. sequence variation) in the absorption, distribution, metabolism, excretion (ADME) and overall efficacy of therapeutic agents is well established. Our ability to identify, interpret and utilize these factors is the subject of much clinical investigation and therapeutic development. However, drug ADME and efficacy are also heavily influenced by epigenetic factors such as DNA/histone methylation and non-coding RNAs [especially microRNAs (miRNAs)]. Results from studies using tools, such as in silico miRNA target prediction, in vitro functional assays, nucleic acid profiling/sequencing and high-throughput proteomics, are rapidly expanding our knowledge of these factors and their effects on drug metabolism. Although these studies reveal a complex regulation of drug ADME, an increased understanding of the molecular interplay between the genome, epigenome and transcriptome has the potential to provide practically useful strategies to facilitate drug development, optimize therapeutic efficacy, circumvent adverse effects, yield novel diagnostics and ultimately become an integral component of personalized medicine. LINKED ARTICLESThis article is part of a themed section on Epigenetics and Therapy. To view the other articles in this section visit http://dx.doi. org/10.1111/bph.2015.172.issue-11 Abbreviations ABC, ATP-binding cassette; ABCB1/MDR1/P-gp, multidrug resistance protein 1/P-glycoprotein; ADME, absorption, distribution, metabolism, excretion; antimiR, miRNA antagonist; CYP450, cytochrome P450; DOX, doxorubicin; ESR1, oestrogen receptor alpha; ETS1, V-Ets avian erythroblastosis virus E26 oncogene homologue 1; GPX7, glutathione peroxidase 7; GSS, glutathione synthetase; HDAC, histone deacetylase; LXRA, liver X receptor α; miRNA, microRNA; mRNA, messenger RNA; ncRNA, non-coding RNA; NR1C1, PPARα; PK, pharmacokinetic; PXR, pregnane X receptor; RISC, RNA-induced silencing complex; RXR, retinoid X receptor; SLC, solute carrier; UGT, UDP-glucuronosyltransferase; UTR, untranslated region; VD receptor, vitamin D receptor The proper control of absorption, distribution, metabolism and excretion (ADME) of xenobiotics is essential for living organisms to obtain energy, acquire necessary building blocks (e.g. essential amino acids) and maintain homeostasis in a complex chemical environment. Genes involved in ADME activities encode various receptor/transporters, biotransformation enzymes and accessory proteins (PharmaADME, http://pharmaadme.org/joomla/). These proteins include membrane transporters responsible for the absorption and excretion of specific molecules and enzymes to convert xenobiotics for excretion. To date, over 300 transporters and enzymes directly involved in ADME process have been described. This long list of components makes the study of ADME inherently complex, as transporters and enzymes work in concert to respond dynamically to diverse external factors. Despite the formidable complexity of the field, an understanding of ADME is critical for drug development in order...

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“…Numerous biological processes, including cell fate determination in embryonic stem cells as well as the regulation of adipogenic and osteogenic differentiation, have been confirmed to be regulated by miRNAs in human bone marrow mesenchymal stem cells (hBMSCs) [11]. Many studies have shown that miR-27 plays important roles in lipid metabolism and adipogenesis [12]. The miR-27 family has two isoforms, intergenic miRNA miR-27a and intronic miRNA miR-27b [13].…”

Section: Introductionmentioning

confidence: 99%

MiR-27b Impairs Adipocyte Differentiation of Human Adipose Tissue-Derived Mesenchymal Stem Cells by Targeting LPL

Hu¹,

Tang²,

Hu³

et al. 2018

Cell Physiol Biochem

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Background/Aims: In this study, the molecular mechanisms of miR-27b and lipoprotein lipase (LPL) that regulate human adipose-derived mesenchymal stem cells (hASCs) adipogenic differentiation were detected. Methods: Microarray analysis was applied to screen for differentially expressed miRNAs and mRNA during hASCs adipocyte differentiation induction. MiR-27b and LPL were found to have abnormal expression. Then, a dual luciferase reporter assay was employed to validate the targeting relationship between miR-27b and LPL. We also utilized qRT-PCR, western blot, cellular immunofluorescence and an oil red O staining assay to analyze the regulation of miR-27b and LPL during adipogenic differentiation. Results: The microarray analysis demonstrated that, during adipogenic differentiation, miR-27b was down-regulated, while LPL was up-regulated but tended to become stable 14 days after induction. A dual luciferase reporter assay confirmed the negative targeting regulatory relationship between miR-27b and LPL. After overexpressing and silencing miR-27b, LPL was found to be reversely regulated by miR-27b according to qRT-PCR and western blot. The fat-formation-related biomarkers CCAAT-enhancer binding protein α (c/EBPα) and peroxisome proliferator-activated receptors γ (PPARγ) had decreasing levels after over-expressing miR-27b or knockdown of LPL followed by adipogenic differentiation. Meanwhile, the oil red O staining assay revealed that the accumulation of lipid droplets decreased. There was no change in the expression of c/EBPα, PPARγ, or lipid droplet accumulation when overexpressing miR-27b and LPL. Conclusion: During the adipogenic differentiation of hASCs, miR-27b expression decreased, and LPL expression increased. The abnormal expression of miR-27b and LPL effectively regulated the adipogenic differentiation of hASCs.

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MicroRNA-27a/b regulates cellular cholesterol efflux, influx and esterification/hydrolysis in THP-1 macrophages

Cited by 161 publications

References 50 publications

Lipoprotein lipase: From gene to atherosclerosis

Lipoprotein lipase: From gene to atherosclerosis

The effects of microRNA on the absorption, distribution, metabolism and excretion of drugs

MiR-27b Impairs Adipocyte Differentiation of Human Adipose Tissue-Derived Mesenchymal Stem Cells by Targeting LPL

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