Overexpression of the FGF-2 24-kDa isoform up-regulates IL-6 transcription in NIH-3T3 cells
Overexpression of the FGF-2 24-kDa isoform up-regulates IL-6 transcription in NIH-3T3 cells
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DOI：
10.1016/s0014-5793(98)01086-2
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发表时间：
1998-09-25
期刊：
影响因子：
3.5
通讯作者：
Faye, JC
中科院分区：
文献类型：
--
作者：
Delrieu, I;Arnaud, E;Faye, JC
我们已经分离出过表达成纤维细胞生长因子（FGF）-2的核24-kDa亚型的NIH-3 T3细胞系，并表征了其对这些细胞中白细胞介素-6（IL-6）表达的调节作用。表达最高水平的克隆pRF 5能够在1%血清培养基中生长到高饱和密度，并获得了辐射抗性优势。在pRF 5和另一个克隆pRF 1中，IL-6 RNA水平仅显著增加。用IL-6启动子构建体的研究表明，IL-6基因上调发生在转录水平，不涉及AP-1结合位点。外源性加入FGF-2的18-kDa亚型（100 ng/ml）可下调IL-6，涉及AP-1结合位点，因此提示细胞内24-kDa亚型的受体非依赖性途径。(C)1998年欧洲生物化学学会联合会。
We have isolated NIH-3T3 cell lines overexpressing the nuclear 24-kDa isoform of fibroblast growth factor (FGF)-2 and characterized its regulatory effect on the expression of interleukin-6 (IL-6) in these cells. The clone pRF5 expressing the highest level was able to grow in 1% serum medium to a high saturation density and acquired a radioresistance advantage. In pRF5 and another clone pRF1, IL-6 RNA levels mere markedly increased. Studies with IL-6 promoter constructs revealed that IL-6 gene up-regulation occurred at the transcriptional level and did not involve the AP-1 binding site. Exogenously added 18-kDa isoform of FGF-2 (100 ng/ml) produced down-regulation of IL-6 involving an AP-1 binding site, thus suggesting a receptor-independent pathway for the intracellular 24-kDa isoform. (C) 1998 Federation of European Biochemical Societies.