Differential Expression of Heat Shock Transcription Factors and Heat Shock Proteins after Acute and Chronic Heat Stress in Laying Chickens (Gallus gallus)

文献类型： 外文期刊

第一作者： Xie, Jingjing

作者： Xie, Jingjing;Tang, Li;Lu, Lin;Zhang, Liyang;Luo, Xugang;Xi, Lin;Liu, Hsiao-Ching;Odle, Jack

作者机构：

期刊名称：PLOS ONE （ 影响因子：3.24； 五年影响因子：3.788 ）

ISSN： 1932-6203

年卷期： 2014 年 9 卷 7 期

页码：

收录情况： SCI

摘要： Heat stress due to high environmental temperature negatively influences animal performances. To better understand the biological impact of heat stress, laying broiler breeder chickens were subjected either to acute (step-wisely increasing temperature from 21 to 35 degrees C within 24 hours) or chronic (32 degrees C for 8 weeks) high temperature exposure. High temperature challenges significantly elevated body temperature of experimental birds (P < 0.05). However, oxidation status of lipid and protein and expression of heat shock transcription factors (HSFs) and heat shock proteins (HSPs) 70 and 90 were differently affected by acute and chronic treatment. Tissue-specific responses to thermal challenge were also found among heart, liver and muscle. In the heart, acute heat challenge affected lipid oxidation (P = 0.05) and gene expression of all 4 HSF gene expression was upregulated (P < 0.05). During chronic heat treatment, the HSP 70 mRNA level was increased (P < 0.05) and HSP 90 mRNA (P < 0.05) was decreased. In the liver, oxidation of protein was alleviated during acute heat challenge (P < 0.05), however, gene expression HSF2, 3 and 4 and HSP 70 were highly induced (P < 0.05). HSP90 expression was increased by chronic thermal treatment (P < 0.05). In the muscle, both types of heat stress increased protein oxidation, but HSFs and HSPs gene expression remained unaltered. Only tendencies to increase were observed in HSP 70 (P = 0.052) and 90 (P = 0.054) gene expression after acute heat stress. The differential expressions of HSF and HSP genes in different tissues of laying broiler breeder chickens suggested that anti-heat stress mechanisms might be provoked more profoundly in the heart, by which the muscle was least protected during heat stress. In addition to HSP, HSFs gene expression could be used as a marker during acute heat stress.

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