Expression pattern of myostatin in gastrocnemius muscle of rats after sciatic nerve crush injury
Expression pattern of myostatin in gastrocnemius muscle of rats after sciatic nerve crush injury
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DOI：
10.1002/mus.20749
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发表时间：
2007-05-01
期刊：
影响因子：
3.4
通讯作者：
Gu, Xiaosong
中科院分区：
文献类型：
--
作者：
Liu, Mei;Zhang, Donglei;Gu, Xiaosong
肌肉生长抑制素是一种强有力的骨骼肌生长抑制因子。本研究的目的是研究肌肉抑制素在失神经诱导的肌肉萎缩过程中的表达谱，以了解肌肉抑制素的表达与肌肉萎缩的关系。建立坐骨神经卡压模型，对大鼠腓肠肌进行形态计量学分析，评价肌肉萎缩程度，并采用实时定量逆转录聚合酶链式反应(RT-PCR)和Western印迹法分别检测神经损伤后不同时间点腓肠肌中myostatin基因和蛋白的表达水平。神经损伤后1~28d肌肉萎缩呈抛物线型变化，14d达高峰。在此期间，myostatin的表达变化相反，1~14d肌肉抑制素基因或蛋白的表达逐渐增加，然后逐渐下降至第28天，达到正常水平。统计分析进一步提供了证据表明，在神经损伤后28天内，肌肉抑制素的表达与肌肉萎缩之间存在显著的负相关。因此，我们的研究描述了肌肉抑制素在一种特定类型的肌肉萎缩中的表达模式，并提出了将其作为未来临床应用的治疗靶点的可能性。
Myostatin is a strong inhibitor of skeletal muscle growth. The purpose of this study was to investigate myostatin expression profiles during denervation-induced muscle atrophy in order to understand the relationship between myostatin expression and muscle atrophy. We constructed a sciatic nerve crush model, undertook morphometric analyses of rat gastrocnemius muscle to evaluate the degree of muscle atrophy, and utilized a real-time quantitative reverse transcription-polymerase chain reaction (RT-PCR) and Western blot analysis to measure myostatin mRNA and protein expression levels, respectively, in the gastrocnemius at different time-points after nerve injury. Muscle atrophy changed in a parabola-like manner from day 1 to day 28 after nerve injury, with a maximum value at day 14. During this time, myostatin expression changed in the reverse manner, with myostatin mRNA or protein expression gradually increasing from days 1-14, and then gradually declining to day 28, when the normal level was reached. Statistical analyses further provided evidence for a significant negative linear correlation between myostatin expression and muscle atrophy within a 28-day period after nerve injury. Our study thus describes the expression pattern of myostatin in response to a specific type of muscle atrophy and raises the possibility of developing myostatin as a therapeutic target for future clinical applications,