Transcriptional profiling of rat skeletal muscle hypertrophy under restriction of blood flow.
Transcriptional profiling of rat skeletal muscle hypertrophy under restriction of blood flow.
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DOI：
10.1016/j.gene.2016.09.008
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发表时间：
2016-12
期刊：
影响因子：
3.5
通讯作者：
Shouyu Xu;Xueyun Liu;Zhenhuang Chen;Gaoquan Li;Qin Chen;Guoqing Zhou;Ruijie Ma;Xinmiao Yao;Xiao Huang
中科院分区：
文献类型：
--
作者：
Shouyu Xu;Xueyun Liu;Zhenhuang Chen;Gaoquan Li;Qin Chen;Guoqing Zhou;Ruijie Ma;Xinmiao Yao;Xiao Huang
低强度阻力训练（LIRT）下的血流限制（BFR）可以对肌肉产生与高强度阻力训练（HIRT）相似的效果，同时克服临床环境中发生的HIRT的许多限制。然而，BFR诱导肌肉肥大的潜在分子机制仍然很大程度上未知。在这里，使用BFR大鼠模型，我们的目的是更好地阐明调节肌肉肥大的机制，由BFR诱导，并揭示可能的临床治疗萎缩的情况下的目标。我们进行了基因组全基因组筛选与微阵列分析，以确定独特的差异表达的基因在大鼠肌肉肥大。然后，我们成功地分离出差异表达的基因从BRF处理比目鱼肌样品通过比较Affyellow大鼠基因组U34 2.0阵列与对照组。采用qRT-PCR和免疫组织化学（IHC）分析了其他相关的差异表达基因。结果表明，BFR诱导的肌肉肥大本质上是由蛋白质周转率调节的。具体而言，PI 3 K/AKT和MAPK途径在控制蛋白质合成中起正调节剂的作用，而泛素-蛋白酶体起负调节剂的作用。这代表了BFR处理后大鼠比目鱼肌中基因表达谱的第一次全基因组水平研究。这可能有助于我们理解调节和控制肌肉肥大的分子机制，并为旨在预防临床环境中肌肉萎缩的BFR策略提供支持。
Blood flow restriction (BFR) under low-intensity resistance training (LIRT) can produce similar effects upon muscles to that of high-intensity resistance training (HIRT) while overcoming many of the restrictions to HIRT that occurs in a clinical setting. However, the potential molecular mechanisms of BFR induced muscle hypertrophy remain largely unknown. Here, using a BFR rat model, we aim to better elucidate the mechanisms regulating muscle hypertrophy as induced by BFR and reveal possible clinical therapeutic targets for atrophy cases. We performed genome wide screening with microarray analysis to identify unique differentially expressed genes during rat muscle hypertrophy. We then successfully separated the differentially expressed genes from BRF treated soleus samples by comparing the Affymetrix rat Genome U34 2.0 array with the control. Using qRT-PCR and immunohistochemistry (IHC) we also analyzed other related differentially expressed genes. Results suggested that muscle hypertrophy induced by BFR is essentially regulated by the rate of protein turnover. Specifically, PI3K/AKT and MAPK pathways act as positive regulators in controlling protein synthesis where ubiquitin-proteasome acts as a negative regulator. This represents the first general genome wide level investigation of the gene expression profile in the rat soleus after BFR treatment. This may aid our understanding of the molecular mechanisms regulating and controlling muscle hypertrophy and provide support to the BFR strategies aiming to prevent muscle atrophy in a clinical setting.