Atrophy, hypertrophy, and hypoxemia induce transcriptional regulators of the ubiquitin proteasome system in the rat heart
Atrophy, hypertrophy, and hypoxemia induce transcriptional regulators of the ubiquitin proteasome system in the rat heart
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DOI：
10.1016/j.bbrc.2006.01.163
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发表时间：
2006-04-07
影响因子：
3.1
通讯作者：
Taegtmeyer, H
中科院分区：
文献类型：
--
作者：
Razeghi, P;Baskin, KK;Taegtmeyer, H
背景资料：在骨骼肌中，调节泛素蛋白酶体系统（UPS）的蛋白质的转录水平随着萎缩而增加，随着肥大而减少。是否同样是真实的心脏Muscle是未知的。目的的研究：我们开始描述的UPS在萎缩，肥大和缺氧诱导的重塑heart.Methods和结果：心脏萎缩诱导大鼠心脏异位移植的转录概况。结扎大鼠升主动脉，造成左心室肥厚。为研究低氧血症对大鼠左心室的影响，采用低压缺氧模型。使用定量RT-PCR测量了六种已知的UPS调节剂的转录水平，泛素B（Ub B）、泛素缀合酶UbcH 2和E2-14 kDa、泛素连接酶Mafbx/Atrogin-1和MuRF-1以及蛋白酶体亚基PSMB 4。卸载诱导的萎缩增加了UbB的mRNA水平，并降低了两种遍在蛋白连接酶的水平。研究的所有UPS基因的转录水平增加在肥厚和缺氧的心脏（E2-14 kDa除外）。结论：心脏萎缩，肥大和低氧血症都增加心肌UbB的表达，这表明UbB是负荷诱导和缺氧介导的心脏重塑的转录标志物。(c)2006年爱思唯尔公司All rights reserved.
Background: In skeletal muscle, transcript levels of proteins regulating the ubiquitin proteasome system (UPS) increase with atrophy and decrease with hypertrophy. Whether the same is true for heart Muscle is not known.Aim of the study: We set out to characterize the transcriptional profile of regulators of the UPS during atrophy-, hypertrophy-, and hypoxia-induced remodeling of the heart.Methods and results: Cardiac atrophy was induced by heterotopic transplantation of the rat heart. Left ventricular hypertrophy was induced by banding of the ascending aorta in rats. To Study the effects of hypoxemia on the left ventricle, rats were exposed to hypobaric hypoxia. Transcript levels of six known regulators of the UPS, ubiquitin B (UbB), the ubiquitin conjugating enzymes UbcH2 and E2-14 kDa, the ubiquitin ligases Mafbx/Atrogin-1 and MuRF-1, and the proteasomal subunit PSMB4 were measured using quantitative RT-PCR. Unloading-induced atrophy increased mRNA levels of UbB and decreased levels of both ubiquitin ligases. Transcript levels of all UPS genes investigated increased in the hypertrophied and hypoxic heart (with the exception of E2-14 kDa).Conclusions: Cardiac atrophy, hypertrophy, and hypoxemia all increase myocardial UbB expression, suggesting that UbB is a transcriptional marker for load-induced and hypoxia-mediated cardiac remodeling. (c) 2006 Elsevier Inc. All rights reserved.