Abstract

Abstract Approximately 90% of beef cattle on feed in the United States receive an anabolic implant during production, which results in increased growth, efficiency, and economic return to producers. However, the molecular mechanism through which these anabolic implants operate to improve skeletal muscle growth remains unknown. The objective of this study was to determine the molecular mechanism through which estradiol (E2) and trenbolone acetate (TBA) improve skeletal muscle growth in beef cattle and to specifically understand whether E2 and/or TBA function by modulating transcription. To address this, bovine satellite cells (BSC) were isolated from three different backgrounded steers and grown in culture. Once cultures reached 75% confluency they were treated with 1% fetal bovine serum (FBS) and 10 nM E2 or 10 nM TBA. In an additional experiment, all previously listed treatments were given in addition to actinomycin D (AD, a non-specific inhibitor of transcription). Treatment with E2 or TBA increased proliferation (P < 0.05) when compared to a 1% FBS control. Furthermore, treatment with E2 or TBA in the presence of AD increased proliferation (P < 0.01) when compared to cultures treated with just AD. These results indicate that TBA and E2 are both capable of increasing proliferation of BSC cultures through non-transcriptional mechanisms. Future work will identify the TBA and E2 signaling pathways that affect muscle growth and don’t involve changes in gene transcription.

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