Abstract

Sex steroid hormones are used in the meat industry due to their ability to regulate muscle hypertrophy. However, the mechanisms underlying their action are not fully elucidated. Recent reports demonstrate that steroid hormones increase oxytocin (OXT) expression in skeletal muscle, indicating that OXT may play a role in satellite cell activity. This hypothesis was tested using steroid hormones (17β-estradiol [E2]; trenbolone acetate [TBA]), tamoxifen (TAM), OXT, and atosiban (A: OXT receptor inhibitor) applied to bovine satellite cells (BSCs) to investigate BSC regulation by OXT. Oxytocin alone increased fusion index (P < 0.05) but not BSC proliferation. Oxytocin reduced (P < 0.05) apoptotic nuclei and stimulated migration rate (P < 0.05). Similarly, E2 and TBA increased (P < 0.05) BSC proliferation rate, fusion index, and migration and decreased (P < 0.05) apoptotic nuclei. 17β-Estradiol or TBA supplemented with A had lower (P < 0.05) BSC proliferation rate, fusion index, and migration and more (P < 0.05) apoptotic nuclei compared with E2 or TBA alone. Furthermore, OXT expression increased (P < 0.05) in E2 or TBA-treated proliferating BSC. Oxytocin, E2, and TBA increased (P < 0.05) MyoD and MyoG expression in proliferating BSC. During BSC differentiation, OXT expression increased (P < 0.05) with E2 or TBA treatments. MyoG expression increased (P < 0.05) in OXT, E2, and TBA compared with control. However, A, OXT + A, TAM, TAM + OXT, E2 + TAM, E2 + A, and TBA + A decreased (P < 0.05) MyoG expression during BSC differentiation. These results indicate that OXT is involved in steroid hormone–stimulated BSC activity.

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