Transcription profiling of different types of skeletal muscles from wild type and alpha tropomyosin transgenic slow mice to investigate the molecular mechanisms implicated in the mouse model of nemaline myopathy

The aim of this study was to investigate the molecular mechanisms implicated in this mouse model of nemaline myopathy, and to further compare the molecular disease response in different skeletal muscles. For this purpose, snap frozen skeletla muscle specimens from wild type and transgenic for alpha tropomyosin slow mice were studied. Five different muscle types were used (diaphragm, plantaris, extensor digitorum longus, tibialis anterior, gastrocnemus). Mice were sacrificed between 7 and 10 months. RNA pools from 3-5 animals were created and each pool was hybridized to a U74Av2 Affymetrix GeneChip. Datasets from 36 GeneChips were included in this study. Experiment Overall Design: 36 skeletal mouse muscle RNA pools were used, from 5 different skeletal muscles, in two different conditions (wild type and transgenic)本研究旨在探究该杆状体肌病（nemaline myopathy）小鼠模型中的分子机制，并进一步比较不同骨骼肌的分子疾病应答反应。为此，我们对野生型及慢型α原肌球蛋白（alpha tropomyosin slow）转基因小鼠的速冻骨骼肌标本进行了研究。本次实验使用5种不同的肌肉组织：膈肌、跖肌、趾长伸肌、胫骨前肌及腓肠肌。实验小鼠于7至10月龄时处死。将3至5只动物的RNA混合为一个样本池，每个样本池均与U74Av2 Affymetrix基因芯片（Affymetrix GeneChip）进行杂交。本研究共纳入36张基因芯片的数据集。实验整体设计如下：使用来自5种不同骨骼肌的36个小鼠骨骼肌RNA样本池，涵盖两种实验条件（野生型与转基因型）