Source:http://linkedlifedata.com/resource/pubmed/id/21291493
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
2011-3-25
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pubmed:abstractText |
1. Adipocyte hypertrophy and hyperplasia are important processes in the development of obesity. To understand obesity and its associated diseases, it is important to elucidate the molecular mechanisms governing adipogenesis. MicroRNA-375 has been shown to inhibit differentiation of neurites, and participate in the regulation of insulin secretion and blood homeostasis. However, it is unknown whether miR-375 plays a role in adipocyte differentiation. 2. To investigate the role of miR-375 in adipocyte differentiation, we compared the miR-375 expression level between 3T3-L1 pre-adipocytes and adipocytes using miRNA microarray and quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR) analysis. Furthermore, we evaluated the effects of overexpression or inhibition of miR-375 on 3T3-L1 adipocyte differentiation. 3. In the present study, we found that miR-375 expression was increased after induction of adipogenic differentiation. Overexpression of miR-375 enhanced 3T3-L1 adipocyte differentiation, as evidenced by its ability to increase mRNA levels of both CCAAT/enhancer binding protein-? (C/EBP?) and peroxisome proliferator-activated receptor-? (PPAR?2), and induction of adipocyte fatty acid-binding protein (aP2) and triglyceride (TG) accumulation. Furthermore, we found overexpression of miR-375 suppressed phosphorylation levels of extracellular signal-regulated kinases 1/2 (ERK1/2). In contrast, anti-miR-375 increased ERK1/2 phosphorylation levels and inhibited mRNA expression of C/EBP?, PPAR?2 and aP2 in 3T3-L1 adipocyte, accompanied by decreased adipocyte differentiation. 4. Taken together, these data suggest that miR-375 promotes 3T3-L1 adipocyte differentiation, possibly through modulating the ERK-PPAR?2-aP2 pathway.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/CCAAT-Enhancer-Binding Protein-alpha,
http://linkedlifedata.com/resource/pubmed/chemical/Extracellular Signal-Regulated MAP...,
http://linkedlifedata.com/resource/pubmed/chemical/Fabp4 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Fatty Acid-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/MicroRNAs,
http://linkedlifedata.com/resource/pubmed/chemical/Mirn375 microRNA, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/PPAR gamma,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Triglycerides,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
1440-1681
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pubmed:author | |
pubmed:copyrightInfo |
© 2011 The Authors. Clinical and Experimental Pharmacology and Physiology © 2011 Blackwell Publishing Asia Pty Ltd.
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pubmed:issnType |
Electronic
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pubmed:volume |
38
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
239-46
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pubmed:meshHeading |
pubmed-meshheading:21291493-3T3-L1 Cells,
pubmed-meshheading:21291493-Adipocytes,
pubmed-meshheading:21291493-Adipogenesis,
pubmed-meshheading:21291493-Animals,
pubmed-meshheading:21291493-CCAAT-Enhancer-Binding Protein-alpha,
pubmed-meshheading:21291493-Cell Differentiation,
pubmed-meshheading:21291493-Extracellular Signal-Regulated MAP Kinases,
pubmed-meshheading:21291493-Fatty Acid-Binding Proteins,
pubmed-meshheading:21291493-MAP Kinase Signaling System,
pubmed-meshheading:21291493-Mice,
pubmed-meshheading:21291493-MicroRNAs,
pubmed-meshheading:21291493-PPAR gamma,
pubmed-meshheading:21291493-RNA, Messenger,
pubmed-meshheading:21291493-Triglycerides,
pubmed-meshheading:21291493-Tumor Necrosis Factor-alpha,
pubmed-meshheading:21291493-Up-Regulation
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pubmed:year |
2011
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pubmed:articleTitle |
MicroRNA-375 promotes 3T3-L1 adipocyte differentiation through modulation of extracellular signal-regulated kinase signalling.
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pubmed:affiliation |
Department of Physiology, School of Medicine, Health Key Laboratory for Pharmacoproteomics of Hunan Province/Institute of Pharmacy and Pharmacology, University of South China, Hengyang, China.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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