首页> 美国卫生研究院文献>BioMed Research International >UHRF1 Promotes Proliferation of Human Adipose-Derived Stem Cells and Suppresses Adipogenesis via Inhibiting Peroxisome Proliferator-Activated Receptor γ
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UHRF1 Promotes Proliferation of Human Adipose-Derived Stem Cells and Suppresses Adipogenesis via Inhibiting Peroxisome Proliferator-Activated Receptor γ

机译:UHRF1促进人类脂肪干细胞的增殖,并通过抑制过氧化物酶体增殖物激活的受体γ抑制脂肪形成。

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摘要

Once the adipose tissue is enlarged for the purpose of saving excess energy intake, obesity may be observed. Ubiquitin-like with PHD and RING Finger domains 1 (UHRF1) is helpful in repairing damaged DNA as it increases the resistance of cancer cells against cytocidal drugs. Peroxisome proliferator-activated receptor γ (PPARγ), an important nucleus transcription factor participating in adipogenesis, has been extensively reported. To date, no study has indicated whether UHRF1 can regulate proliferation and differentiation of human adipose-derived stem cells (hADSCs). Hence, this study aimed to utilize overexpression or downregulation of UHRF1 to explore the possible mechanism of proliferation and differentiation of hADSCs. We here used lentivirus, containing UHRF1 (LV-UHRF1) and siRNA-UHRF1 to transfect hADSCs, on which Cell Counting Kit-8 (CCK-8), cell growth curve, colony formation assay, and EdU proliferation assay were applied to evaluate proliferation of hADSCs, cells cycle was investigated by flow cytometry, and adipogenesis was detected by Oil Red O staining and Western blotting. Our results showed that UHRF1 can promote proliferation of hADSCs after overexpression of UHRF1, while proliferation of hADSCs was reduced through downregulation of UHRF1, and UHRF1 can control proliferation of hADSCs through transition from G1-phase to S-phase; besides, we found that UHRF1 negatively regulates adipogenesis of hADSCs via PPARγ. In summary, the results may provide a new insight regarding the role of UHRF1 on regulating proliferation and differentiation of hADSCs.
机译:一旦为了节省过多的能量摄入而扩大了脂肪组织,就可以观察到肥胖。具有PHD和RING指域1(UHRF1)的泛素样蛋白有助于修复受损的DNA,因为它增加了癌细胞对杀细胞药物的抵抗力。过氧化物酶体增殖物激活受体γ(PPARγ),一种参与脂肪形成的重要核转录因子,已被广泛报道。迄今为止,尚无研究表明UHRF1是否能调节人脂肪干细胞(hADSCs)的增殖和分化。因此,本研究旨在利用UHRF1的过表达或下调来探索hADSCs增殖和分化的可能机制。我们在这里使用包含UHRF1(LV-UHRF1)和siRNA-UHRF1的慢病毒转染hADSCs,在其上应用Cell Counting Kit-8(CCK-8),细胞生长曲线,集落形成测定和EdU增殖测定来评估增殖对hADSCs的细胞,通过流式细胞术研究细胞周期,并通过油红O染色和Western印迹检测脂肪形成。我们的结果表明,UHRF1可以在过表达UHRF1后促进hADSCs的增殖,而通过下调UHRF1来降低hADSCs的增殖,而UHRF1可以通过从G1期过渡到S期来控制hADSCs的增殖。此外,我们发现UHRF1通过PPAR γ负调控hADSCs的脂肪生成。总之,这些结果可能会提供有关UHRF1在调节hADSCs增殖和分化中作用的新见解。

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