Low temperature exposure inhibits proliferation and induces apoptosis of bovine subcutaneous preadipocytes via p38 MAPK/JNK activation.

Abstract

Cold stress can cause changes in cell growth states. Cell proliferation and apoptosis are important physiological processes to maintain normal growth and development of cells and tissues. We sought to identify the impact of low temperature exposure on bovine subcutaneous preadipocyte proliferation and apoptosis. We first cultured preadipocytes at different low temperatures (35°C, 33°C, and 31°C) for 12h, and then at 31°C for 24 and 48h. The results showed that compared with the 37°C group, exposure to 31°C significantly reduced cell viability and number as well as inhibited cell cycle progression in preadipocytes. Moreover, low temperature also significantly upregulated the apoptosis rate of preadipocytes. After low temperature treatment, the mRNA levels of Cyclin E, CDK2 and B-cell lymphoma 2 (Bcl-2) were decreased in preadipocytes, whereas that of p53, p21 and Bcl-2 associated x protein (Bax) were increased in preadipocytes. Concurrently, low temperature increased the proteins levels of p53, Bax and Cleaved Caspase3, and reduced the protein level of Bcl-2 in preadipocytes. Furthermore, the elevated phosphorylation levels of p38 mitogen-activated protein kinases (p38 MAPK) and c-jun NH2-terminal kinase (JNK) were detected in cold-treated preadipocytes. The influence of low temperature exposure on preadipocyte proliferation and apoptosis were obviously weakened after blocking the p38 MAPK and JNK signaling pathways. In conclusion, low temperature exposure could inhibit proliferation and cell cycle progression and induce apoptosis through activation of p38 MAPK and JNK signaling pathways in bovine subcutaneous preadipocytes.