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    C2 skeletal myoblast survival, death, proliferation and differentiation: regulation by Adra1d

    Saini, Amarjit, Al-Shanti, Nasser and Stewart, Claire E. (2010) C2 skeletal myoblast survival, death, proliferation and differentiation: regulation by Adra1d. Cellular Physiology and Biochemistry, 25 (2-3). pp. 253-262. ISSN 1421-9778

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    IGF-I positively impacts on muscle anabolism/regeneration. Using C2 skeletal myoblasts, we previously reported high dose TNF-α -induced (10 ng.ml-1) cell death is rescued by IGF-I. However, non-myotoxic low dose TNF-α (1.25 ng.ml-1) elicits a MAPK-mediated apoptotic response when co-incubated with IGF-I (1.5 ng.ml-1). Our aim was to investigate these conflicting roles of IGF-I in our model. Insulin array and qRT-PCR identified Adra1d as a potential regulatory gene that was up-regulated in survival and down-regulated under apoptotic conditions. TNF-α administration (1.25 or 10 ng.ml-1) induced significant decreases (∼50% both incubations) in Adra1d expression relative to DM. IGF-I addition to high dose TNF-α (10 ng.ml-1) induced myoblast survival and matched a significant (P < 0.05) increase in Adra1d expression. By contrast, IGF-I addition to low dose TNF-α (1.25 ng.ml-1) induced elevated death resulting in a significant (P < 0.05) decline (∼55%) in Adra1d expression. Pre-administration of PD98059 (20 uM), which rescues death induced by co-incubation of low dose TNF-α with IGF-I, Adra1d levels were again comparable to DM control. Since Adra1d was elevated following incubations that induced myoblast survival, we investigated effects of Adra1d siRNA gene silencing under these conditions. Adra1d knockdown resulted in significantly higher levels of cell death under all incubations suggesting Adra1d expression is essential for skeletal muscle cell survival.

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