MicroRNA-375 promotes 3T3-L1 adipocyte differentiation through modulation of extracellular signal-regulated kinase signalling.
MicroRNA-375 promotes 3T3-L1 adipocyte differentiation through modulation of extracellular signal-regulated kinase signalling.
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DOI：
10.1111/j.1440-1681.2011.05493.x
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发表时间：
2011-04
影响因子：
2.9
通讯作者：
Liao DF
中科院分区：
文献类型：
--
作者：
Ling HY;Wen GB;Feng SD;Tuo QH;Ou HS;Yao CH;Zhu BY;Gao ZP;Zhang L;Liao DF
脂肪细胞的肥大和增生是肥胖发生发展的重要过程。为了了解肥胖及其相关疾病，阐明脂肪形成的分子机制是非常重要的。MiR-375已被证明抑制神经突的分化并参与胰岛素分泌和血液稳态的调节。然而，目前还不清楚miR-375是否在脂肪细胞分化中发挥作用。为了研究miR-375在脂肪细胞分化中的作用，我们使用miRNA微阵列和定量实时RT-PCR（qRT-PCR）分析比较了3 T3-L1前脂肪细胞和脂肪细胞中miR-375的表达水平。此外，我们评估了过表达或抑制miR-375对3 T3-L1脂肪细胞分化的影响。在这项研究中，我们发现miR-375的表达在诱导成脂分化后增加。miR-375过表达增强3 T3-L1脂肪细胞分化：通过其增加CCAAT/增强子结合蛋白α（C/EBPα）和过氧化物酶体增殖物激活受体γ 2（PPARγ2）的mRNA水平以及诱导脂肪细胞脂肪酸结合蛋白（aP 2）和甘油三酯（TG）积累的能力证明。此外，我们发现过表达miR-375抑制细胞外信号调节激酶1/2（ERK 1/2）的磷酸化水平。与此相反，Anti-miR-375可增加3 T3-L1脂肪细胞中ERK 1/2磷酸化水平，抑制C/EBPα、PPARγ2和aP 2 mRNA表达，同时降低脂肪细胞分化。综上所述，这些数据表明miR-375促进3 T3-L1脂肪细胞分化，可能通过调节ERK-PPAR γ2 -aP 2途径。
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. MiR-375 has been demonstrated 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. To investigate the role of miR-375 in adipocyte differentiation, we compared miR-375 expression level between 3T3-L1 pre-adipocytes and adipocytes using miRNA microarray and quantitative real-time RT-PCR (qRT-PCR) analysis. Furthermore, we evaluated the effects of overexpression or inhibition of miR-375 on 3T3-L1 adipocyte differentiation. In this 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 proteinα (C/EBPα) and peroxisome proliferator-activated receptor gamma (PPARγ2) 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/EBPα, PPARγ2 and aP2 in 3T3-L1 adipocyte, accompanied by decreased adipocyte differentiation. Taken together, these data suggest that miR-375 promotes 3T3-L1 adipocyte differentiation, possibly via modulating ERK - PPARγ2 - aP2 pathway.
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影响因子：
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作者：
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通讯作者：
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通讯作者：
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