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The COP9 signalosome has a role in adipogenesis

机译:COP9信号组在adipoonesis中具有作用

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Obesity is one of the most serious health problems of the 21st century. The expansion of fat tissue requires angiogenesis, which needs the vascular endothelial growth factor (VEGF), a protein controlled by the COP9 signalosome (CSN). Methods: LiSa-2 cell line was used as a model for adipogenesis. Insulin (INS), cortisol (COR) and triiodthyronine (T3) stimulated the differentiation of LiSa-2 adipogenesis. Ten uM of curcumin (CUR) were used to inhibit the CSN and to block VEGF production. LiSa-2 cells were transfected with siCSN5 and CSN5wt or CSN5 mutant. VEGF production was quantified by ELISA. Changes of regulatory proteins were assessed by Western blotting. Results: CUR affected protein levels of p53 and c-Jun in LiSa-2 cells moderately. However, the VEGF production was significantly reduced. Overex-pression of CSN5 increased the VEGF production by 30%, whereas downregulation of CSN5 led to a reduction of VEGF. Conclusion: The CSN is a potential regulator of adipogenesis.
机译:肥胖是21世纪最严重的健康问题之一。脂肪组织的膨胀需要血管生成,这需要血管内皮生长因子(VEGF),由COP9信号组(CSN)控制的蛋白质。方法:使用Lisa-2细胞系作为脂肪发生模型。胰岛素(INS),皮质醇(COR)和三碘(T3)刺激了LISA-2脂肪发生的分化。用于抑制CSN的十个姜黄素(CUR)并阻止VEGF生产。用SICSN5和CSN5WT或CSN5突变体转染LISA-2细胞。 VEGF生产由ELISA量化。通过蛋白质印迹评估调节蛋白的变化。结果:患有含量含量的P53和C-Jun中等蛋白质水平。然而,VEGF生产明显减少。 CSN5的过度压力将VEGF产生增加30%,而CSN5的下调导致VEGF的减少。结论:CSN是脂肪发生的潜在调节因子。

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