Short-term exercise does not increase ER stress protein expression in cardiac muscle
Short-term exercise does not increase ER stress protein expression in cardiac muscle
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DOI：
10.1249/mss.0b013e3180cc25c7
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发表时间：
2007-09-01
期刊：
影响因子：
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通讯作者：
Powers, Scott K.
中科院分区：
文献类型：
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作者：
Murlasits, Zsolt;Lee, Youngil;Powers, Scott K.
目的：短期（连续三至五天）和长期（数周至数月）耐力运动训练均可提供心脏保护作用，防止缺血再灌注 (IR) 引起的损伤。然而，运动引起的心脏保护机制尚不清楚。新的证据表明，内质网 (ER) 损伤会导致红外线引起的心肌损伤。由此可见，运动诱导的 ER 应激蛋白表达可以作为运动诱导的心脏保护免受 IR 损伤的介质。因此，这些实验检验了运动训练与心脏内质网应激蛋白增加相关的假设。方法：成年雄性 Sprague-Dawley 大鼠（N = 13）习惯在跑步机上跑步 5 天，然后连续几天进行 5 次每次 60 分钟的运动（类似于 VO2max 的 70%）。通过标准组织学（氯化三苯基四唑 (TTC) 方法）确定 IR 引起的梗塞面积。通过蛋白质印迹分析心脏内质网应激蛋白 Grp78、Grp94 和钙网蛋白的水平。此外，我们还测定了热休克蛋白 72 (HSP72) 以及与细胞损伤相关的内质网蛋白（包括 CHOP、半胱天冬酶 12、Puma、Noxa 和 ATF3）的心肌水平。结果：我们的运动方案得出了然而，运动训练并没有增加（P > 0.05）心脏内质网应激蛋白、Grp78、Grp94 和钙网蛋白的水平。 Noxa 或 ATF3 结论：这些数据表明短期运动训练不会升高心脏中的 ER 应激蛋白，因此短期运动训练的心脏保护作用似乎与 ER 应激适应无关。
Purpose: Both short-term (three to five consecutive days) and long-term (weeks to months) endurance exercise training provides cardioprotection against ischemia-reperfusion (IR)-induced injury. However, the mechanisms responsible for exercise-induced cardioprotection are not well understood. Emerging evidence indicates that endoplasmic reticulum (ER) damage contributes to IR-induced myocardial injury. It follows that exercise-induced expression of ER stress proteins could serve as the mediators of exercise-induced cardioprotection against IR injury. Hence, these experiments tested the hypothesis that exercise training is associated with an increase in ER stress proteins in the heart. Methods: Adult male Sprague-Dawley rats (N = 13) were habituated to treadmill running for 5 d, followed by five 60-min exercise bouts (similar to 70% of VO2max) on consecutive days. Infarct area resulting from IR was determined by a standard histological (triphenyltetrazolium chloride (TTC) method. Cardiac levels of ER stress proteins Grp78, Grp94, and calreticulin were analyzed via Western blot. Moreover, we determined myocardial levels of heat shock protein 72 (HSP72) along with ER proteins associated with cellular injury, including CHOP, caspase 12, Puma, Noxa, and ATF3. Results: Our exercise protocol resulted in cardioprotection as evidenced by reduced infarct size (P < 0.05) and increased myocardial HSP72 levels (+227%; P < 0.01) in the exercise-trained animals. Nonetheless, exercise training did not increase (P > 0.05) cardiac levels of the ER stress proteins, Grp78, Grp94, and calreticulin. Moreover, exercise did not alter myocardial levels of CHOP, caspase 12, Puma, Noxa, or ATF3. Conclusion: These data reveal that short-term exercise training does not elevate ER stress proteins in the heart. Hence, the cardioprotective effect of short-term exercise training does not seem to be linked to ER stress adaptation.