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首页> 外文期刊>Molecular and Cellular Biology >Complex regulation of transforming growth factor beta 1, beta 2, and beta 3 mRNA expression in mouse fibroblasts and keratinocytes by transforming growth factors beta 1 and beta 2.
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Complex regulation of transforming growth factor beta 1, beta 2, and beta 3 mRNA expression in mouse fibroblasts and keratinocytes by transforming growth factors beta 1 and beta 2.

机译：通过转化生长因子beta 1和beta 2复杂调节小鼠成纤维细胞和角质形成细胞中转化生长因子beta 1，beta 2和beta 3 mRNA的表达。

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Regulation of transforming growth factor beta 1 (TGF beta 1), TGF beta 2, and TGF beta 3 mRNAs in murine fibroblasts and keratinocytes by TGF beta 1 and TGF beta 2 was studied. In quiescent AKR-2B fibroblasts, in which TGF beta induces delayed stimulation of DNA synthesis, TGF beta 1 autoregulation of TGF beta 1 expression was observed as early as 1 h, with maximal induction (25-fold) after 6 to 12 h. Increased expression of TGF beta 1 mRNA was accompanied by increased TGF beta protein production into conditioned medium of AKR-2B cells. Neither TGF beta 2 nor TGF beta 3 mRNA, however, was significantly induced, but both were apparently down regulated at later times by TGF beta 1. Protein synthesis was not required for autoinduction of TGF beta 1 mRNA in AKR-2B cells. Nuclear run-on analyses and dactinomycin experiments indicated that autoregulation of TGF beta 1 expression is complex, involving both increased transcription and message stabilization. In contrast to TGF beta 1, TGF beta 2 treatment of quiescent AKR-2B cells increased expression of TGF beta 1, TGF beta 2, and TGF beta 3 mRNAs, but with different kinetics. Autoinduction of TGF beta 2 mRNA occurred rapidly with maximal induction at 1 to 3 h, enhanced TGF beta 3 mRNA levels were observed after 3 h, and increased expression of TGF beta 1 occurred later, with maximal mRNA levels obtained after 12 to 24 h. Nuclear run-on analyses indicated that TGF beta 2 regulation of TGF beta 2 and TGF beta 3 mRNA levels is transcriptional, while TGF beta 2 induction of TGF beta 1 expression most likely involves both transcriptional and posttranscriptional controls. In BALB/MK mouse keratinocytes, minimal autoinduction of TGF beta 1 occurred at only the 12- and 24-h time points and protein synthesis was required for this autoinduction. The results of this study provide an example in which TGF beta 1 and TGF beta 2 elicit different responses and demonstrate that expression of TGF beta 1, and TGF beta 3 are regulated differently. The physiological relevance of TGF beta 1 autoinduction in the context of wound healing is discussed.
机译：研究了转化生长因子β1（TGFβ1），TGFβ2和TGFβ3 mRNA在鼠成纤维细胞和角质形成细胞中对TGFβ1和TGFβ2的调节作用。在静止的AKR-2B成纤维细胞中，TGFβ诱导DNA合成的延迟刺激，最早在1 h观察到TGFβ1对TGFβ1表达的自动调节，在6至12 h后最大程度地诱导（25倍）。 TGFβ1mRNA表达的增加伴随着进入AKR-2B细胞条件培养基的TGFβ蛋白产生的增加。然而，TGF beta 2和TGF beta 3 mRNA均未得到明显诱导，但两者在以后的时间里都明显被TGF beta 1下调。在AKR-2B细胞中自动诱导TGF beta 1 mRNA不需要蛋白质合成。核实验分析和放线菌素实验表明，TGFβ1表达的自动调节非常复杂，涉及转录增加和信息稳定。与TGF beta 1相比，静止AKR-2B细胞的TGF beta 2处理增加了TGF beta 1，TGF beta 2和TGF beta 3 mRNA的表达，但是具有不同的动力学。 TGFβ2mRNA的自诱导迅速发生，在1至3 h达到最大诱导，在3 h后观察到TGF beta 3 mRNA的水平升高，TGF beta 1的表达增加，随后在12至24 h达到最大mRNA水平。核运行分析表明，TGFβ2对TGFβ2和TGFβ3 mRNA水平的调节是转录的，而TGFβ2对TGFβ1表达的诱导最有可能涉及转录和转录后控制。在BALB / MK小鼠角质形成细胞中，仅在12小时和24小时的时间点发生了最小的TGFβ1自动诱导，并且这种自动诱导需要蛋白质合成。这项研究的结果提供了一个示例，其中TGF beta 1和TGF beta 2引起不同的反应，并证明TGF beta 1和TGF beta 3的表达受到不同的调节。讨论了伤口愈合过程中TGFβ1自诱导的生理相关性。

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