Damage to the myogenic differentiation of C2C12 cells by heat stress is associated with up-regulation of several selenoproteins
Abstract
This study was conducted to profile the selenoprotein encoding genes or proteins in mouse C2C12 cells and integrate their roles in the skeletal cell damage induced by heat stress (HS). Cells were cultured at 37.0 °C or 41.5 °C for 4, 6 or 8 days. The mRNA expression of 24 selenoprotein encoding genes and abundance of 5 selenoproteins were investigated. HS suppressed myogenic differentiation and impaired the development of muscle myotubes. HS down-regulated (P < 0.01) mRNA abundance of MYOD and MYOGENIN, and decreased (P < 0.01) MYOGENIN protein expression, HS elevated (P < 0.01) HSP70 and (P < 0.01) the ratio of BCL-2 to BAX at both mRNA and protein level. Meanwhile, HS up-regulated (P < 0.01-0.05) expressions of 18, 11 and 8 selenoprotein encoding genes after 4, 6 and 8 days of hyperthermia, and only down-regulated (P < 0.01) DIO2 after 6 and 8 days of hyperthermia, respectively. Furthermore, HS influenced expression of selenoproteins and up-regulated (P < 0.01-0.05) GPX1, GPX4 and SEPN1 after 6 days of HS. The damage to development of mouse skeletal muscle myotubes by HS accompanied with the up-regulation of both selenoprotein encoding genes and proteins, which suggested a potential protective effect of selenoprotein on hyper...Continue Reading
References
Effect of heat stress on oxidative stress, lipid peroxidation and some stress parameters in broilers
The heat shock protein 70 family: Highly homologous proteins with overlapping and distinct functions
The FoxO3/type 2 deiodinase pathway is required for normal mouse myogenesis and muscle regeneration.
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