Heat shock protects L6 myotubes from catabolic effects of dexamethasone and prevents downregulation of NF-kappaB.
Heat shock protects L6 myotubes from catabolic effects of dexamethasone and prevents downregulation of NF-kappaB.
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热休克可保护 L6 肌管免受地塞米松分解代谢的影响，并防止 NF-kappaB 下调。
DOI：
10.1152/ajpregu.2001.281.4.r1193
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发表时间：
2001
期刊：
影响因子：
--
通讯作者：
Hasselgren,PO
中科院分区：
文献类型：
--
作者：
Luo,G;Sun,X;Hungness,E;Hasselgren,PO
糖皮质激素是各种分解代谢条件下肌肉恶病质的最重要介质。最近的研究表明，转录因子NF-κB作为泛素-蛋白酶体蛋白水解途径中基因的抑制因子，糖皮质激素通过下调NF-κB活性来增加肌肉蛋白水解。热休克（应激）反应，其特征在于诱导热休克蛋白，赋予对各种有害刺激的保护作用。在本研究中，我们验证了热休克反应保护肌细胞免受地塞米松的分解代谢作用并阻止NF-κB下调的假设。对培养的L 6肌管进行热休克（43°C，1小时），然后在37°C下恢复1小时。此后，用1 μM地塞米松处理细胞6 h，在此期间，以[3 H]酪氨酸预标记蛋白质释放的TCA可溶性放射性测定蛋白质降解。热休克导致热休克蛋白70的蛋白质和mRNA水平增加。地塞米松诱导的蛋白质降解的增加在表达热休克反应的细胞中被阻止。在相同的细胞中，地塞米松诱导的NF-κB DNA结合活性下调被阻断。目前的结果表明，热休克反应可以保护肌肉细胞免受地塞米松的分解代谢作用，这种作用可能与抑制NF-κB活性下调有关。
Glucocorticoids are the most important mediator of muscle cachexia in various catabolic conditions. Recent studies suggest that the transcription factor NF-κB acts as a suppressor of genes in the ubiquitin-proteasome proteolytic pathway and that glucocorticoids increase muscle proteolysis by downregulating NF-κB activity. The heat shock (stress) response, characterized by the induction of heat shock proteins, confers a protective effect against a variety of harmful stimuli. In the present study, we tested the hypothesis that the heat shock response protects muscle cells from the catabolic effects of dexamethasone and prevents downregulation of NF-κB. Cultured L6 myotubes were subjected to heat shock (43°C for 1 h) followed by recovery at 37°C for 1 h. Thereafter, cells were treated for 6 h with 1 μM dexamethasone, during which period protein degradation was measured as release of TCA-soluble radioactivity from proteins that had been prelabeled with [3H]tyrosine. Heat shock resulted in increased protein and mRNA levels for heat shock protein 70. The increase in protein degradation induced by dexamethasone was prevented in cells expressing the heat shock response. In the same cells, dexamethasone-induced downregulation of NF-κB DNA binding activity was blocked. The present results suggest that the heat shock response may protect muscle cells from the catabolic effects of dexamethasone and that this effect of heat shock may be related to inhibited downregulation of NF-κB activity.
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DOI：
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发表时间：
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