Fig. 8

Pictorial representation of C2C12 myoblast cell differentiation up to 8 days under normoxia and hypoxia with/without S1P pretreatment. S1P pretreatment facilitated the C2C12 myoblast differentiation under both normoxia and hypoxia via remodulated S1PR mRNA expression, altered myokine secretion, increased intracellular calcium and improved energy generation via boosting the aerobic/anaerobic metabolism and mitochondrial mass. Under normoxia, all of these led to a robust increase in myotubular branching and thickness following S1P pretreatment. Hypoxia exposure, an extreme stress, led to derangement of the S1PR_1–3 expression and impaired differentiation as evident from disturbed surrogate markers of differentiation leading to formation of thin and short nascent myofibers. However, S1P pretreatment prior to hypoxia exposure showed partial recovery from hypoxia-compromised differentiation with relatively longer myofibers and at least scantily developed nascent myotubes