Barash Ilona A, Mathew Liby, Lahey Michele, Greaser Marion L, Lieber Richard L
Deptartment of Orthopaedics, Veterans Affairs Medical Center and Univ. of California, San Diego, 3350 La Jolla Village Drive, San Diego, CA 92161, USA.
Am J Physiol Cell Physiol. 2005 Nov;289(5):C1312-20. doi: 10.1152/ajpcell.00117.2005. Epub 2005 Aug 10.
Muscle LIM protein (MLP) has been suggested to be an important mediator of mechanical stress in cardiac tissue, but the role that it plays in skeletal muscle remains unclear. Previous studies have shown that it is dramatically upregulated in fast-to-slow fiber-type transformation and also after eccentric contraction (EC)-induced muscle injury. The functional consequences of this upregulation, if any, are unclear. In the present study, we have examined the skeletal muscle phenotype of MLP-knockout (MLPKO) mice in terms of their response to EC-induced muscle injuries. The data suggest that while the MLPKO mice recover completely after EC-induced injury, their torque production lags behind that of heterozygous littermates in the early stages of the recovery process. This lag is accompanied by decreased expression of the muscle regulatory factor MyoD, suggesting that MLP may influence gene expression. In addition, there is evidence of type I fiber atrophy and a shorter resting sarcomere length in the MLPKO mice, but no significant differences in fiber type distribution. In summary, MLP appears to play a subtle role in the maintenance of normal muscle characteristics and in the early events of the recovery process of skeletal muscle to injury, serving both structural and gene-regulatory roles.
肌肉LIM蛋白（MLP）被认为是心脏组织机械应力的重要介质，但其在骨骼肌中的作用仍不清楚。先前的研究表明，在快肌纤维向慢肌纤维类型转变以及离心收缩（EC）诱导的肌肉损伤后，MLP会显著上调。这种上调的功能后果（如果有的话）尚不清楚。在本研究中，我们从对EC诱导的肌肉损伤的反应方面，研究了MLP基因敲除（MLPKO）小鼠的骨骼肌表型。数据表明，虽然MLPKO小鼠在EC诱导的损伤后能完全恢复，但在恢复过程的早期，它们的扭矩产生落后于杂合子同窝小鼠。这种滞后伴随着肌肉调节因子MyoD表达的降低，表明MLP可能影响基因表达。此外，有证据表明MLPKO小鼠存在I型纤维萎缩和静息肌节长度缩短，但纤维类型分布没有显著差异。总之，MLP似乎在维持正常肌肉特征以及骨骼肌损伤恢复过程的早期事件中发挥着微妙作用，兼具结构和基因调节作用。
