Department of Biophysics and Human Physiology, Medical University of Warsaw, Warsaw, Poland.
J Physiol Pharmacol. 2009 Dec;60(4):157-62.
The serum level of the transforming growth factor-beta1 (TGF-beta1) is elevated after acute bouts of exercise and prolonged training, as well as after myocardial infarction. However, the source of this increase remains unclear. Contracting skeletal muscles are known to be the source of many cytokines. To determine whether skeletal or heart muscles produce TGF-beta1 during exercise, we investigated the effect of a single bout of acute exercise on TGF-beta1 generation in skeletal and heart muscles in untrained rats (UT, n=30) and in rats subjected to prolonged (6-week) endurance training (T, n=29). The UT and T (a day after final training) groups were subjected to an acute bout of exercise with the same work load. Rats from both groups were sacrificed and skeletal and heart muscle samples were collected before (pre), immediately after (0 h), or 3 hours (3 h) after acute exercise. TGF-beta1 mRNA was quantified by RT-PCR in these samples, and basal TGF-beta1 protein levels were determined in skeletal muscle in the UTpre and Tpre subgroups by ELISA. Acute exercise caused a non-significant increase in TGF-beta1 mRNA in skeletal muscle in UT0h rats, in compare to UTpre rats. There was a significant decrease of TGF-beta1 mRNA in the T0h group (p=0.0013) in compare to Tpre rats. Prolonged training caused a significant increase in TGF-beta1 mRNA (p=0.02); however, the TGF-beta1 protein level decreased (p=0.02). In heart muscle, there was a significant decrease of TGF-beta1 mRNA in UT0h (p=0.01) and UT3h (p=0.04) compared to UTpre rats. TGF-beta1 mRNA levels were unchanged in T0h and T3h compared to Tpre; basal TGF-beta1 mRNA expression after training was also unchanged (UTpre vs. Tpre). We conclude that physical exercise is a potent stimulus for inducing TGF-beta1 gene expression in skeletal muscle, but does not increase the protein level. Thus, skeletal and heart muscle do not contribute to increased serum levels of TGF-beta1 after physical exercise.
血清转化生长因子-β1（TGF-β1）水平在急性运动和长期训练后以及心肌梗死后升高。然而，这种增加的来源尚不清楚。众所周知，收缩的骨骼肌是许多细胞因子的来源。为了确定在运动过程中是骨骼肌还是心肌产生 TGF-β1，我们研究了单次急性运动对未经训练的大鼠（UT，n=30）和经过 6 周耐力训练的大鼠（T，n=29）的骨骼肌和心肌中 TGF-β1 产生的影响。UT 和 T（最后一次训练后一天）组接受了相同负荷的急性运动。两组大鼠均处死，采集运动前（pre）、运动即刻（0 h）或运动后 3 小时（3 h）的骨骼肌和心肌样本。通过 RT-PCR 定量这些样本中的 TGF-β1 mRNA，并通过 ELISA 测定 UTpre 和 Tpre 亚组中骨骼肌中的基础 TGF-β1 蛋白水平。与 UTpre 大鼠相比，UT0h 大鼠的骨骼肌中 TGF-β1 mRNA 有非显著性增加。与 Tpre 大鼠相比，T0h 组的 TGF-β1 mRNA 显著减少（p=0.0013）。长期训练导致 TGF-β1 mRNA 显著增加（p=0.02）；然而，TGF-β1 蛋白水平下降（p=0.02）。在心肌中，与 UTpre 大鼠相比，UT0h（p=0.01）和 UT3h（p=0.04）的 TGF-β1 mRNA 显著减少。与 Tpre 相比，T0h 和 T3h 时 TGF-β1 mRNA 水平不变；训练后基础 TGF-β1 mRNA 表达也不变（UTpre 与 Tpre）。我们得出结论，运动是诱导骨骼肌中 TGF-β1 基因表达的有效刺激因素，但不会增加蛋白水平。因此，运动后骨骼肌和心肌不会导致 TGF-β1 血清水平升高。
