Differential gene expression in the rat soleus muscle during early work overload‐induced hypertrophy

• Published in: The FASEB journal 2002-02, Vol.16 (2), p.1-21
• Main Authors: Carson, J. A., Nettle, D., Reecy, J. M.
• Format: Article
• Language: English
• Subjects: Animals; Chemokines - genetics; Extracellular Matrix Proteins - genetics; Gene Expression Profiling; Gene Expression Regulation, Enzymologic - genetics; Growth Substances - genetics; Hypertrophy - genetics; Immunity, Innate - genetics; messenger ribonucleic acid; muscle hypertrophy; Muscle, Skeletal - metabolism; Muscle, Skeletal - pathology; Physical Exertion - physiology; Rats; RNA, Messenger - genetics; RNA, Messenger - metabolism; Signal Transduction - genetics; soleus; Transcription Factors - genetics
• ISSN: 0892-6638; 1530-6860
• DOI: 10.1096/fj.01-0544fje

ABSTRACT Delineating the molecular mechanisms that are responsive to work overload is crucial to understanding the adaptive processes controlling skeletal muscle mass. We have examined the molecular events associated with increased workload by using microarray analysis to begin to define the mechanotransduction responsive transcription programs in skeletal muscle. Microarray analysis identified 112 mRNAs that were expressed differentially in the soleus muscle of sham‐operated vs. gastrocnemius‐ablated rats. These genes can be classified into cell proliferation, autocrine/paracrine, extracellular matrix, immune response, intracellular signaling, metabolism, neural, protein synthesis/degradation, structural, and transcription. These findings dramatically increase the number of known, differentially expressed mRNA during early skeletal muscle hypertrophy. In toto, our findings indicate that work overload induced skeletal muscle hypertrophy alters autocrine/paracrine signaling, intracellular signaling, and transcription factor expression, which likely results in a dramatic change in cellular metabolism, cell proliferation, and muscle structure. These data enhance our understanding of the complex molecular mechanisms controlling skeletal muscle mass in response to increased physical activity.