4.7 Article

Endocrine Signals Altered by Heat Stress Impact Dairy Cow Mammary Cellular Processes at Different Stages of the Dry Period

期刊

ANIMALS
卷 11, 期 2, 页码 -

出版社

MDPI
DOI: 10.3390/ani11020563

关键词

apoptosis; autophagy; hormones; gene expression

资金

  1. USDA-National Institute for Food and Agriculture (Washington, DC) [2015-67015-23409]

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Late-gestation heat stress alters gene expression in the mammary gland, impacting key cellular processes and potentially disrupting mammary gland remodelling by modulating estrogen and prolactin signalling, leading to reduced milk yield in the subsequent lactation. Further research is needed to uncover the mechanisms behind production impairments caused by late-gestation heat stress.
Simple Summary Late-gestation heat stress increases blood prolactin and decreases oestrogen concentrations in dry cows. These hormonal alterations may disturb mammary gland remodelling during the dry period, thereby being potentially responsible for the observed production impairments during the subsequent lactation. This project aimed to better understand the molecular mechanisms underlying subsequent impairments in mammary performance after dry period heat stress. For this, we studied the expression of genes encompassing prolactin and oestrogen pathways and key cellular process pathways under different thermal environments and in vitro hormonal milieus. The results of this study revealed that late-gestation heat stress impacted the expression of genes in the mammary gland involved in key cellular processes occurring during the dry period. Furthermore, our results indicated that these modifications are in part modulated by alterations of oestrogen and prolactin signalling. Hormonal alterations occurring under late gestation heat stress may disturb mammary gland remodelling, resulting in a reduced milk yield during the subsequent lactation. We investigated the effects of an altered endocrine environment on mammary gene expression at different stages of the dry period. Mammary gland biopsies from in vivo-cooled (CL) or heat-stressed (HT) cows were collected at d 3 and 35 relative to dry-off and divided into explants. Explants were incubated in vitro for 24 h in one of three media: Basal: no prolactin or estrogen; CL-mimic: Basal + low prolactin + high 17 beta-estradiol, or HT-mimic: Basal + high prolactin + low 17 beta-estradiol. Real time qPCR was used to quantify gene expression. We established that late-gestation heat stress changes the expression of prolactin and oestrogen receptors, downregulates genes involved in apoptosis, autophagy and proliferation at d 3 and upregulates genes related to those cellular processes at d 35. Moreover, compared with in vivo treatments, we showed that the expression of fewer genes was impacted by in vitro treatments which aimed to mimic the hormonal response of cows exposed to a different environment. Further research will continue to uncover the mechanisms behind the production impairments caused by late-gestation heat stress.

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