Heat stress inhibits proliferation, promotes growth, and induces apoptosis in cultured Lantang swine skeletal muscle satellite cells

Abstract

Proliferation suppression and apoptosis are the prominent characteristics induced by heat stress (HS) in cells, whereas the effects of HS on cell growth (mass accumulation) are unknown. In this study, Lantang swine (an indigenous breed of China) skeletal muscle satellite cells (SCs) were pre-cultured at 37 °C for 24 h. The HS group was subjected to HS at 41 °C, while the control group was maintained at 37 °C. Heat shock protein 70 (HSP70) expression and SC size are significantly increased (P<0.05) by HS, but cell proliferation is suppressed (P<0.05) and apoptosis is induced (P<0.05). HS led to a lower percentage of SCs in the G0/G1 phase (P<0.05) together with a higher percentage of SCs in the S phase (P<0.05). However, the percentage of SCs in the G2/M phase was decreased (P<0.05) at 48 h but then increased (P<0.05) at 72 h with HS. In addition, the phosphorylation ratios of protein kinase b (Akt), ribosomal protein S6 kinase (S6K), and ribosomal protein S6 were increased (P<0.05) by HS. Nevertheless, the phosphorylation ratios of the 4E binding protein 1 and the eukaryotic initiation factor-4E were indistinguishable (P>0.05) from those of the control group. The phosphorylation ratio of the mammalian target of rapamycin (mTOR) (Ser(2448)) increased (P<0.05) within 48 h, and apparent differences were abrogated at 72 h (P>0.05). Moreover, cleaved caspase-3 expression was increased at 72 h (P<0.05). These findings indicate that HS induces apoptosis and disrupts cell cycle distribution to decrease the number of cells. Additionally, HS can promote SC growth via an activated Akt/mTOR/S6K signaling pathway.

Wnt/β‐catenin‐mediated heat exposure inhibits intestinal epithelial cell proliferation and stem cell expansion through endoplasmic reticulum stress

“…Our study showed that exposure to 41°C significantly inhibited the IPEC‐J2 cell proliferation, especially S‐phase cells, which was supported by a decrease in the percentage of EdU + cells and the expression of proliferation marker gene PCNA. This result is consistent with previous studies, that is, high temperature (≥41°C) induces cell damage (Alemu et al, 2018; Gao et al, 2015; Homma & Fujii, 2016; Varasteh et al, 2018; Yang, He, & Zheng, 2007). Of note, a proper increase of temperatures, such as 39°C or 40°C, can improve the viability of porcine intestinal epithelial cells, which might be related to the relatively high resting physiologic body temperature of pigs.…”

Satellite cell activation and apoptosis in skeletal muscle from severely burned children

“…Thermal stress disrupts the cell cycle and induces apoptosis of cultured myoblasts (Gao et al . ), and in the current study we observe DNA damage in satellite cells that is characteristic of apoptosis. Nine of the twelve burn patients displayed evidence (TUNEL+/Pax7+ satellite cell frequency above zero) for satellite cell apoptosis, and the frequency of TUNEL+ satellite cells was significantly correlated with the severity of the burn injury, both in the %TBSA and the %TBSA for 3rd degree burns.…”

“…; Gao et al . ), implying dysregulated terminal activation of satellite cells in the presence of systemic factors induced by burn injury. The fact that burn serum reduces differentiation and fusion of myoblasts cultured in the presence of burn serum implies impairments in the later stages of satellite cell activation.…”

“…Reductions in the satellite cell pool, whether due to apoptosis or inappropriate cell cycle distribution (Gao et al . ), highlight deficiencies in the myogenic response to burn injury (Song et al . ).…”

“…), and heat stress inhibits proliferation and induces apoptosis of cultured primary myoblasts (Gao et al . ). Although the balance between protein anabolism and catabolism largely dictates burn‐induced cachexia (Biolo et al .…”