Beating affects the posttranscriptional regulation of alpha-myosin mRNA in cardiac cultures.

Beating affects the posttranscriptional regulation of alpha-myosin mRNA in cardiac cultures.
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搏动影响心脏培养物中 α-肌球蛋白 mRNA 的转录后调节。

DOI:
10.1152/ajpheart.1996.271.6.h2584
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发表时间:
1996
期刊:
The American journal of physiology.
影响因子:
--
通讯作者:
Russell,B
Russell,B
中科院分区:
--
文献类型:
--
作者:
Goldspink,PH;Thomason,DB;Russell,B

文献摘要

被引文献

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心肌细胞收缩停止导致α-肌球蛋白重链(MHC)mRNA丰度增加,但α-MHC蛋白含量降低。我们的目的是确定转录后机制调节α-MHC mRNA-蛋白解偶联在培养的新生大鼠心脏在收缩活动改变。通过使用维拉帕米(10 μ mol/l;一种Ca(2+)通道阻滞剂)或2,3-丁二酮单肟(5 mmol/l;一种跨桥抑制剂)来阻止自发收缩的心肌细胞。用鹅膏蕈碱(0.5 mumol/l)抑制转录可使正常搏动的肌细胞中的α-MHC mRNA降至最低基线。然而,α-MHC mRNA并没有下降,鹅膏蕈碱处理的非跳动的心肌细胞低。同时,当搏动被阻断时,α-MHC mRNA向较重的多核糖体复合物转移。总之,这些数据表明,收缩停滞调节α-MHC mRNA丰度转录后稳定的翻译延伸阶段的消息。这些转录后调控步骤依赖于跳动本身,而不依赖于Ca 2+进入。
Contractile arrest of cardiac myocytes results in increased abundance of alpha-myosin heavy chain (MHC) mRNA but decreased alpha-MHC protein content. Our aim is to determine the posttranscriptional mechanisms regulating alpha-MHC mRNA-protein uncoupling in cultured neonatal rat hearts during altered contractile activity. Spontaneously contracting myocytes were arrested by the use of verapamil (10 mumol/l; a Ca(2+)-channel blocker) or by 2,3-butanedione monoxime (5 mmol/l; a cross-bridge inhibitor). Inhibition of transcription with amanitin (0.5 mumol/l) decreased the alpha-MHC mRNA in normally beating myocytes to a minimal baseline. However, the alpha-MHC mRNA did not fall this low in amanitin-treated nonbeating myocytes. Concurrently, the alpha-MHC mRNA shifted toward a heavier polysome complex when beating was blocked. Together, these data suggest that contractile arrest regulates alpha-MHC mRNA abundance posttranscriptionally by stabilizing the message at the elongation phase of translation. These posttranscriptional regulatory steps are dependent on beating itself and are independent of Ca2+ entry.