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首页> 外文期刊>Journal of Cachexia, Sarcopenia and Muscle >p62/SQSTM1 but not LC3 is accumulated in sarcopenic muscle of mice
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p62/SQSTM1 but not LC3 is accumulated in sarcopenic muscle of mice

机译：p62 / SQSTM1而不是LC3积累在小鼠的肌肉减少症中

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Abstract Aim We investigated the pathway of autophagy signaling linked to sarcopenia of mice. Methods Young adult (3-month) and aged (24- month) C57BL/6J mice were used. Using real-time PCR, Western blotting, and immunohistochemical microscopy, we evaluated the amounts of p62/SQSTM1, LC3, and Beclin-1 in the quadriceps muscle change with aging in mice. Results Marked fiber atrophy (30%) and many fibers with central nuclei were observed in the aged mice. Western blotting using homogenate of the cytosolic fraction clearly showed that the amounts of p62/SQSTM1 and Beclin-1 proteins were significantly increased in the aged skeletal muscle. The amounts of these proteins in both nuclear and membrane fractions did not change significantly with age. Immunofluorescence labeling indicated that aged mice more frequently possessed p62/SQSTM1-positive fibers in the cytosol in quadriceps muscle than young ones (aged: 14% vs. young: 1%). In aged muscle, p62/SQSTM1-positive fibers were significantly smaller than the surrounding p62/SQSTM1-negative fibers. Aging did not elicit significant changes in the mRNA levels of p62/SQSTM1 and Beclin-1, but decreased LC3 mRNA level. In aged muscle, the location of p62/SQSTM1 immunoreactivity was similar to that of Beclin-1 protein, but not LC3. Conclusion Sarcopenia in mice appears to include a marked defect of autophagy signaling.
机译：摘要目的研究自噬信号传导与小鼠少肌症相关的途径。方法使用成年（3个月）和大龄（24个月）的C57BL / 6J小鼠。使用实时PCR，蛋白质印迹和免疫组织化学显微镜，我们评估了随着衰老小鼠股四头肌肌肉中p62 / SQSTM1，LC3和Beclin-1的含量。结果在老年小鼠中观察到明显的纤维萎缩（30％）和许多具有中心核的纤维。使用细胞质部分匀浆的蛋白质印迹法清楚地表明，老年骨骼肌中p62 / SQSTM1和Beclin-1蛋白的量显着增加。这些蛋白质在核和膜级分中的含量均不会随着年龄的增长而显着变化。免疫荧光标记表明，老年小鼠比年轻小鼠更频繁地在股四头肌的细胞质中拥有p62 / SQSTM1阳性纤维（年龄：14％对年轻：1％）。在衰老的肌肉中，p62 / SQSTM1阳性纤维明显小于周围的p62 / SQSTM1阴性纤维。衰老并没有引起p62 / SQSTM1和Beclin-1 mRNA水平的显着变化，但降低了LC3 mRNA水平。在老年肌肉中，p62 / SQSTM1免疫反应的位置与Beclin-1蛋白相似，但与LC3相似。结论小鼠肌肉减少症似乎包括自噬信号传导的明显缺陷。

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