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首页> 外文期刊>Biochimica et biophysica acta. Molecular basis of disease: BBA >Depletion of Jmjd1c impairs adipogenesis in murine 3T3-L1 cells
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Depletion of Jmjd1c impairs adipogenesis in murine 3T3-L1 cells

机译：JMJD1C的耗尽损害鼠3T3-L1细胞中的脂肪组织

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摘要

Differentiation of adipocytes is a highly regulated process modulated by multiple transcriptional co-activators and co-repressors. JMJD1C belongs to the family of jumonji C (jmjC) domain-containing histone demethylases and was originally described as a ligand-dependent co-activator of thyroid hormone and androgen receptors. Here, we explored the potential role of Jmjdlc in white adipocyte differentiation. To investigate the relevance of Jmjdlc in adipogenesis, murine 3T3-L1 preadipocyte cells with transient knock-down of Jmjdlc (3T3_Jmjdlc) were generated. Depletion of Jmjdlc led to the formation of smaller lipid droplets, reduced accumulation of triglycerides and maintenance of a more fibroblast-like morphology after adipocyte differentiation. Concomitantly, insulin stimulated uptake of glucose and fatty acids was significantly reduced in 3T3_Jmjdlc adipocytes. In line with these observations we detected lower expression of key genes associated with lipid droplet formation (Plinl, Plin4, Cidea) and uptake of glucose and fatty acids (Glut4, Fatpl, Fatp4, Aqp7) respectively. Finally, we demonstrate that depletion of Jmjdlc interferes with mitotic clonal expansion (MCE), increases levels of H3K9me2 (dimethylation of lysine 9 of histone H3) at promotor regions of adipogenic transcription factors (C/EBPs and PPARy) and leads to reduced induction of these key regulators. In conclusion, we have identified Jmjdlc as a modulator of adipogenesis. Our data suggest that Jmjdlc may participate in MCE and the activation of the adipogenic transcription program during the induction phase of adipocyte differentiation in 3T3-L1 cells.
机译：脂肪细胞的分化是由多个转录共激振活化剂和共压制式调节的高度调节过程。 JMJD1C属于含Jumonji C（JMJC）域的组蛋白脱甲基酶的系列，最初被描述为甲状腺激素和雄激素受体的配体依赖性共激活剂。在这里，我们探讨了JMJDLC在白色adipocyte分化中的潜在作用。为了探讨JMJDLC在脂肪发生中的相关性，产生了JMJDLC（3T3_JMJDLC）的瞬态截止的鼠3T3-L1前脂肪细胞细胞。 JMJDLC的耗尽导致形成较小的脂液滴，减少甘油三酯的积累和在脂肪细胞分化后的更加成纤维细胞样形态的维持。同时，3T3_JMJDLC脂肪细胞显着降低了胰岛素刺激的葡萄糖和脂肪酸的吸收。符合这些观察，我们检测了与脂质液滴形成（PLIN1，PLIN4，CIDEA）和葡萄糖和脂肪酸摄取的关键基因的表达分别分别摄取（GLUT4，TATP1，FATP4，AQP7）。最后，我们证明JMJDLC的耗尽干扰有丝分裂克隆膨胀（MCE），在脂肪转录因子（C / EBP和PPARA）的促进区，增加H3K9ME2（组蛋白H3的赖氨酸9的二甲基化），并导致诱导诱导这些关键调节器。总之，我们已经确定了JMJDLC作为脂肪发生的调节剂。我们的数据表明，JMJDLC可以参与MCE和在3T3-L1细胞中脂肪细胞分化的诱导阶段期间激活脂肪转录程序。

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