CCAAT/enhancer binding protein expression is rapidly extinguished in TA1 adipocyte cells treated with tumor necrosis factor.
CCAAT/enhancer binding protein expression is rapidly extinguished in TA1 adipocyte cells treated with tumor necrosis factor.
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DOI：
10.1210/mend.6.7.1508226
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发表时间：
1992-07
影响因子：
--
通讯作者：
Paul Mickey Williams;D. Chang;Ulrich Danesch;Gordon M. Ringold;Renu A. Heller
中科院分区：
文献类型：
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作者：
Paul Mickey Williams;D. Chang;Ulrich Danesch;Gordon M. Ringold;Renu A. Heller
肿瘤坏死因子（TNF）已被证明对多种细胞类型具有不同的作用。在小鼠成脂TA 1细胞系中，TNF完全消除分化并将完全分化的脂肪细胞恢复为成纤维细胞。这种分化阻滞及其逆转是由于脂肪特异性基因表达的快速减少。本研究报告，转录因子，CCAAT/增强子结合蛋白（C/EBP），以前报道，以促进3 T3-L1脂肪细胞的分化，在TA 1细胞中表达。在它们在培养物中的生长期间，C/EBP的水平，如其特定mRNA、蛋白质和DNA结合活性的细胞水平所证明的，当细胞达到汇合并继续分化时显著增加。向培养的前脂肪细胞或完全分化的脂肪细胞中加入TNF可迅速降低C/EBP水平，并伴有脂肪特异性基因表达的降低。C/EBP结合位点存在于几个脂肪特异性基因中，并且在此证明其存在于一个新的脂肪特异性基因克隆47（也称为FSP 27）中，可能是TNF对克隆47（FSP 27）启动子连接的氯霉素乙酰转移酶基因表达的强烈下调的原因。这项研究提出，C/EBP响应TNF治疗的损失可能在一定程度上解释了脂肪细胞分化状态的损失。
Tumor necrosis factor (TNF) has been shown to have diverse effects on a wide variety of cell types. In the mouse adipogenic TA1 cell line, TNF completely abolishes differentiation and reverts fully differentiated fat cells into fibroblasts. This block in differentiation and its reversal is due to the rapid reduction in the expression of adipose-specific genes. This study reports that the transcription factor, CCAAT/enhancer binding protein (C/EBP), previously reported to promote the differentiation of 3T3-L1 adipocytes, is expressed in TA1 cells. During their growth in culture, the levels of C/EBP, as evidenced by its cellular levels of specific mRNA, protein, and DNA binding activity, increase dramatically when cells reach confluence and proceed to differentiate. Addition of TNF to cultured preadipocytes or fully differentiated adipocytes rapidly reduces C/EBP levels and is accompanied by the decrease in expression of adipose-specific genes. C/EBP binding sites occur in several adipose-specific genes, and here it is demonstrated that its presence in a novel adipose-specific gene, Clone 47, also referred to as FSP27, may be responsible for the strong down-regulation of the expression of the Clone 47 (FSP27) promoter-linked chloramphenicol acetyl transferase gene by TNF. This study proposes that the loss of C/EBP in response to TNF treatment may in part explain the loss of the adipocyte differentiated state.