Acute exercise induced changes in rat skeletal muscle mRNAs and proteins regulating type IV collagen content

Acute exercise induced changes in rat skeletal muscle mRNAs and proteins regulating type IV collagen content
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DOI:
10.1152/ajpregu.2001.280.5.r1292
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发表时间:
2001-05-01
影响因子:
2.8
通讯作者:
Takala, TES
Takala, TES
中科院分区:
医学3区
文献类型:
--
作者:
Koskinen, SOA;Wang, W;Takala, TES

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本实验验证了这一假设,即大鼠骨骼肌跑步引起的损伤导致基底膜IV型胶原蛋白的合成和降解以及调节其降解的蛋白质的变化。在下坡跑后6 h或1、2、4或7 d采集比目鱼肌和股四头肌(MQF)红色和白色部分的样本。肌肉β-葡萄糖醛酸酶活性增加表明MQF红色部分的肌肉损伤大于MQF或比目鱼肌的白色部分。在MQF的红色部分中,IV型胶原蛋白表达在翻译前水平上调,蛋白浓度降低,而基质金属蛋白酶-2(MMP-2)(一种降解IV型胶原蛋白的蛋白质)和金属蛋白酶组织抑制剂-2(TIMP-2)(一种抑制降解的蛋白质)在mRNA和蛋白水平平行增加。Ⅳ型胶原mRNA在MQF的白色部分和比目鱼肌中表达增加。MQF的白色部分的蛋白质浓度增加,而比目鱼肌中的蛋白质浓度不变。MMP-2和TIMP-2仅在MQF的白色部分和比目鱼肌中有轻微变化。这些变化似乎取决于肌纤维损伤的严重程度,因此可能反映了基底膜化合物的重组。
This experiment tested the hypothesis that running-induced damage to rat skeletal muscle causes changes in synthesis and degradation of basement membrane type IV collagen and to proteins regulating its degradation. Samples from soleus muscle and red and white parts of quadriceps femoris muscle (MQF) were collected 6 h or 1, 2, 4, or 7 days after downhill running. Increased muscle beta -glucuronidase activity indicated greater muscle damage in the red part of MQF than in the white part of MQF or soleus. In the red part of MQF, type IV collagen expression was upregulated at the pretranslational level and the protein concentration decreased, whereas matrix metalloproteinase-2 (MMP-2), a protein that degrades type IV collagen, and tissue inhibitor of metalloproteinase-2 (TIMP-2), a protein that inhibits degradation, were increased in parallel both at mRNA and protein levels. Type IV collagen mRNA level increased in the white part of MQF and soleus muscle. The protein concentration increased in the white part of MQF and was unchanged in soleus muscle. MMP-2 and TIMP-2 changed only slightly in the white part of MQF and soleus muscle. The changes seem to depend on the severity of myofiber injury and thus probably reflect reorganization of basement membrane compounds.