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

机译:产蛋鸡急性和慢性热应激后热休克转录因子和热休克蛋白的差异表达

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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°C within 24 hours) or chronic (32°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.
机译:高环境温度引起的热应激会对动物的行为产生负面影响。为了更好地了解热应激的生物学影响,对产蛋鸡进行了急性暴露(24小时内逐步将温度从21°C升高到35°C)或慢性暴露(32°C 8周)的高温暴露。高温挑战显着提高了实验禽的体温(P <0.05)。但是,脂质和蛋白质的氧化状态以及热休克转录因子(HSF)和热休克蛋白(HSP)70和90的表达受急性和慢性治疗的影响不同。在心脏,肝脏和肌肉中也发现了对热挑战的组织特异性反应。在心脏中,急性热刺激影响脂质氧化(P = 0.05),所有4种HSF基因表达的基因表达均上调(P <0.05)。在慢性热处理过程中,HSP 70 mRNA水平升高(P <0.05),HSP 90 mRNA水平降低(P <0.05)。在肝脏中,急性热刺激过程中蛋白质的氧化被减轻(P <0.05),但是,基因表达的HSF2、3和4以及HSP 70被高度诱导(P <0.05)。慢性热处理使HSP90表达增加(P <0.05)。在肌肉中,两种类型的热应激均会增加蛋白质氧化,但HSF和HSPs的基因表达仍保持不变。急性热应激后,HSP 70(P = 0.052)和90(P = 0.054)基因表达仅观察到增加的趋势。 HSF和HSP基因在蛋鸡种不同组织中的差异表达表明,抗热应激机制可能在心脏中被更深刻地激发,在热应激中,肌肉受到的保护最少。除了HSP外,HSFs基因表达还可以用作急性热应激期间的标记。

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