Heat shock factor 2 is activated during mouse heart development.
Heat shock factor 2 is activated during mouse heart development.
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DOI：
10.1387/ijdb.11032181
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发表时间：
2000-08
期刊：
影响因子：
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通讯作者：
M. Eriksson;Eero Jokinen;Lea Sistonen;S. Leppä
中科院分区：
文献类型：
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作者：
M. Eriksson;Eero Jokinen;Lea Sistonen;S. Leppä
热休克转录因子家族的两个成员，HSF 1和HSF 2，已被鉴定为哺乳动物热休克基因表达的激活因子。HSF 1是一种经典的应激反应因子，而HSF 2可能在胚胎发生中发挥作用，因为它在小鼠胚胎发育的前和后植入期长达15.5天。在这项研究中，我们分析了HSF 1和HSF 2的表达和激活在小鼠心脏形成。我们的研究结果表明，HSF 1在整个心脏发育过程中表达丰富。相反，在E11.5-12.5发育的小鼠心脏中，选择性剪接的HSF 2-α和HSF 2-β以及另外的更高分子量同种型的表达强烈上调，在该阶段之后，管状心脏已经成环并且形成腔室，并且心肌壁正在成熟并且瓣膜正在分化。在同一发育阶段，HSF 2 DNA结合活性是瞬时诱导的，而在整个心脏发育过程中检测到的弱HSE结合活性主要由HSF 1组成。有趣的是，热休克基因的表达与HSF 2的表达和激活没有时间或空间相关性。两者合计，我们的研究结果表明，HSF 2激活与心脏形成的特定阶段，但不参与诱导热休克基因表达的调节。
Two members of the heat shock transcription factor family, HSF1 and HSF2, have been identified as activators of mammalian heat shock gene expression. HSF1 acts as a classical stress-responsive factor, whereas HSF2 might play a role in embryogenesis, since it is active during pre- and post-implantation periods up to 15.5 days of mouse embryonic development. In this study, we analyzed HSF1 and HSF2 expression and activation during mouse heart formation. Our results show an abundant expression of HSF1 throughout heart development. In contrast, expression of the alternatively spliced HSF2-alpha and HSF2-beta, and an additional higher molecular weight isoform is strongly upregulated in the developing mouse heart at E11.5-12.5, a stage after which tubular heart has looped and chambers formed, and the myocardial walls are maturating and the valves differentiating. At the same developmental stage, HSF2 DNA-binding activity is transiently induced, whereas the weak HSE-binding activity, which is detected throughout heart development, consists primarily of HSF1. Interestingly, heat shock gene expression shows no temporal or spatial correlation with HSF2 expression and activation. Taken together, our results indicate that HSF2 activation is associated with specific stages of heart formation but is not involved in the regulation of inducible heat shock gene expression.