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首页> 外文期刊>American Journal of Physiology >Transcriptional regulation of the type I myosin heavy chain promoter in inactive rat soleus.
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Transcriptional regulation of the type I myosin heavy chain promoter in inactive rat soleus.

机译：非活动大鼠比目鱼肌中I型肌球蛋白重链启动子的转录调控。

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摘要

Chronic muscle inactivity with spinal cord isolation (SI) decreases expression of slow type I myosin heavy chain (MHC) while increasing expression of the faster MHC isoforms, primarily IIx. The purpose of this study was to determine whether type I MHC downregulation in the soleus muscle of SI rats is regulated transcriptionally and to identify cis-acting elements or regions of the rat type I MHC gene promoter involved in this response. One week of SI significantly decreased in vivo activity of the -3500-, -408-, -299-, -215-, and -171-bp type I MHC promoters. The activity of all tested deletions of the type I MHC promoter, relative to the human skeletal alpha-actin promoter, were significantly reduced in the SI soleus, except activity of the -171-bp promoter, which increased. Mutation of the betae3 element (-214/-190 bp) in the -215- and -408-bp promoters and deletion of this element (-171-bp promoter) attenuated type I downregulation with SI. Gel mobility shift assays demonstrated a decrease in transcription enhancer factor-1 binding to the betae3 element with SI, despite an increase in total binding to this region. These results demonstrate that type I MHC downregulation with SI is transcriptionally regulated and suggest that interactions between transcription enhancer factor-1 and the betae3 element are likely involved in this response.
机译：慢性肌无力与脊髓分离（SI）会降低慢速I型肌球蛋白重链（MHC）的表达，同时会增加较快的MHC亚型（主要是IIx）的表达。这项研究的目的是确定SI大鼠比目鱼肌中I型MHC下调是否受到转录调控，并确定参与该反应的大鼠I型MHC基因启动子的顺式作用元件或区域。 SI的一个星期显着降低了-3500-，-408-，-299-，-215-和-171-bp I型MHC启动子的体内活性。相对于人骨骼α-肌动蛋白启动子，所有测试的I型MHC启动子缺失的活性在比目鱼肌中均显着降低，除了-171-bp启动子的活性增加。 -215-和-408-bp启动子中betae3元件的突变（-214 / -190 bp）和该元件（-171-bp启动子）的缺失减弱了SI的I型下调。凝胶迁移率迁移分析表明，尽管与该区域的总结合增加，但转录增强因子-1与SI结合到betae3元件上的结合减少。这些结果表明，SI对I型MHC的下调受到转录调节，并表明转录增强因子1和betae3元素之间的相互作用可能参与了该反应。

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