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首页> 外文期刊>Molecular and Cellular Biology >Interleukin-11 mRNA stabilization in phorbol ester-stimulated primate bone marrow stromal cells.
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Interleukin-11 mRNA stabilization in phorbol ester-stimulated primate bone marrow stromal cells.

机译：佛波酯刺激的灵长类动物骨髓基质细胞中白细胞介素11 mRNA的稳定性。

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12-O-Tetradecanoylphorbol-13-acetate (TPA) stimulation of PU-34 cells, a primate bone marrow stromal cell line, resulted in a prolonged elevation of interleukin-11 (IL-11) mRNA, which can be inhibited by protein synthesis inhibitors. Nuclear run-on assays and actinomycin D experiments demonstrated that the up-regulation of IL-11 gene expression is mainly controlled at the posttranscriptional level through the protein kinase C (PKC) pathway. Inhibition of PKC activity by calphostin C generated an IL-11 mRNA degradation intermediate in TPA-stimulated PU-34 cells. This intermediate retains the 5' untranslated region (5'UTR) and coding region of the IL-11 mRNA but has lost the poly(A) tail and the 3'UTR. The mechanisms underlying IL-11 mRNA stabilization were further investigated by transfections with a variety of chimeric IL-11 constructs and deletion mutants. Two important observations were made from these transient expression experiments: (i) the same 3'UTR of IL-11 mRNA shown to confer instability in one chimeric transcript may not function as a destabilizer in another chimeric RNA, and (ii) the 5'UTR, coding region, and 3'UTR all contribute to IL-11 mRNA decay, and labile IL-11 deletion transcripts are not necessarily stabilized by TPA stimulation. Our study suggests that multiple regions within the IL-11 mRNA are involved in TPA-stimulated IL-11 mRNA stabilization, possibly through a unique RNA folding conformation involving interactions of various RNA sequences within the IL-11 mRNA molecule.
机译：12-O-Tetradecanoylphorphor-13-乙酸盐（TPA）刺激PU-34细胞（灵长类骨髓基质细胞系）导致白介素11（IL-11）mRNA的延长升高，可以通过蛋白质合成来抑制抑制剂。核运行试验和放线菌素D实验表明，IL-11基因表达的上调主要通过蛋白激酶C（PKC）途径控制在转录后水平。钙磷蛋白C抑制PKC活性在TPA刺激的PU-34细胞中产生IL-11 mRNA降解中间体。该中间体保留IL-11 mRNA的5'非翻译区（5'UTR）和编码区，但丢失了poly（A）尾巴和3'UTR。通过用多种嵌合IL-11构建体和缺失突变体进行转染，进一步研究了IL-11 mRNA稳定的基本机制。从这些瞬时表达实验中获得了两个重要的观察结果：（i）相同的IL-11 mRNA的3'UTR在一个嵌合转录物中表现出不稳定性，可能不会在另一个嵌合RNA中起到去稳定剂的作用，并且（ii）5' UTR，编码区和3'UTR都有助于IL-11 mRNA的降解，不稳定的IL-11缺失转录本不一定通过TPA刺激而稳定下来。我们的研究表明，IL-11 mRNA内的多个区域可能参与了TPA刺激的IL-11 mRNA稳定化，可能是通过涉及IL-11 mRNA分子内各种RNA序列相互作用的独特RNA折叠构象。

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