Transcription Factor 21 Promotes Chicken Adipocyte Differentiation at Least in Part via Activating MAPK/JNK Signaling.
Transcription Factor 21 Promotes Chicken Adipocyte Differentiation at Least in Part via Activating MAPK/JNK Signaling.
复制标题
转录因子 21 至少部分通过激活 MAPK/JNK 信号传导促进鸡脂肪细胞分化
作者：
Zhang X;Cheng B;Jiang H;Liu C;Cao Z;Luan P;Wang N;Li H
转录因子21（TCF 21）调控鸡脂肪形成的分子机制尚不清楚。因此，本研究旨在研究TCF 21对鸡脂肪形成的影响的信号通路。本研究使用永生化鸡前脂肪细胞系（ICP）、稳定过表达TCF 21的前脂肪细胞系（LV-TCF 21）和对照前脂肪细胞系（LV-对照）。我们发现，与LV对照相比，LV-TCF 21中c-Jun N-末端激酶（JNK）的磷酸化显著升高。用JNK抑制剂SP 600125处理ICP细胞后，ICP细胞分化受到抑制，表现为脂滴积聚减少，过氧化物酶体增殖物激活受体γ（PPARγ）、CCAAT/增强子结合蛋白α（C/EBPα）、脂肪细胞脂肪酸结合蛋白（A-FABP）和脂蛋白脂酶（LPL）表达减少。此外，我们发现SP 600125对JNK的抑制显著削弱了TCF 21驱动脂肪形成的能力。综上所述，我们的研究结果表明，TCF 21促进脂肪细胞的分化，至少部分通过激活MAPK/JNK途径。
The molecular mechanisms of transcription factor 21 (TCF21) in regulating chicken adipogenesis remain unclear. Thus, the current study was designed to investigate the signaling pathway mediating the effect of TCF21 on chicken adipogenesis. Immortalized chicken preadipocytes cell line (ICP), a preadipocyte cell line stably overexpressing TCF21 (LV-TCF21) and a control preadipocyte cell line (LV-control) were used in the current study. We found that the phosphorylation of c-Jun N-terminal kinases (JNK) was significantly elevated in LV-TCF21 compared to LV-control. After treating ICP cells with a JNK inhibitor SP600125, the differentiation of ICP was inhibited, as evidenced by decreased accumulation of lipid droplets and reduced expression of peroxisome proliferator-activated receptor γ (PPARγ), CCAAT/enhancer binding protein α (C/EBPα), adipocyte fatty acid binding protein (A-FABP), and lipoprotein lipase (LPL). Moreover, we found that the inhibition of JNK by SP600125 remarkably impaired the ability of TCF21 to drive adipogenesis. Taken together, our results suggest that TCF21 promotes the differentiation of adipocytes at least in part via activating MAPK/JNK pathway.
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