Author:
Hu Han,Wang Jiaqi,Gao Haina,Li Songli,Zhang Yangdong,Zheng Nan
Abstract
The objective of this study was to identify the apoptosis and cell-defence response of bovine mammary epithelial cells under heat stress (HS). Cells were exposed to either 38°C or 42°C for 0.5, 1, 3, 5, 8, or 12 h, and the transcription of heat shock proteins (Hsps), Bcl-2 family, caspases and apoptosis-regulated genes were quantified by quantitative real-time polymerase chain reaction. Caspase-3, -7 and -8 were markedly upregulated by HS and the peak gene abundance appeared at 5 h. However, the same family numbers, caspase-6 and -9 were sustained downregulated in HS. The expression of anti-apoptotic gene Bcl-2, Bcl-2A and Mcl-1 increased sharply in HS but returned to pre-HS levels after 8 h. The pro-apoptotic genes: Bax, Bak and Bid were downregulated during HS. The striking changes of signalling factors of apoptosis: tumour necrosis factor receptor, p53, Apaf-1 was upregulated, and Fas was downregulated in HS. Stress proteins Hsp genes (hsp27, hsp70 and hsp90) were generally increased at 42°C and this was especially apparent for hsp70 transcription as it was increased 14-fold at 1 h. Simultaneously, HS induced cell apoptosis, and the peak of apoptosis rate appeared at 3 and 5 h, which were assessed by flow cytometry. Our results suggest that HS induces cell apoptosis, disturbs the normal biological activity, and aroused intracellular thermotolerance responses of bovine mammary epithelial cells.
Subject
Animal Science and Zoology,Food Science
Cited by
22 articles.
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