Abstract
Maternal heat stress induced the aberrant epigenetic patterns resulting in the abnormal development of offspring embryos. It is unclear whether maternal dietary manganese supplementation as an epigenetic modifier could protect the chick embryonic development against maternal heat stress via epigenetic mechanisms. To test this hypothesis using an avian model, a completely randomized design with a 2 (maternal normal and high environmental temperatures of 21 and 32°C, respectively) × 3 (maternal dietary manganese sources, the control diet without manganese supplementation and the control diet + 120 mg/kg as either inorganic or organic manganese) factorial arrangement was adopted. Maternal environmental hyperthermia increased mRNA expressions of heat shock proteins 90 and 70, cyclin-dependent kinase 6 and B-cell CLL/lymphoma 2-associated X protein displaying oxidative damage and apoptosis in the embryonic heart. Maternal environmental hyperthermia impaired the embryonic development associated with the alteration of epigenetic status, as evidenced by global DNA hypomethylation and histone 3 lysine 9 hypoacetylation in the embryonic heart. Maternal dietary manganese supplementation increased the heart anti-apoptotic gene B-cell CLL/lymphoma 2 expressions under maternal environmental hyperthermia and manganese superoxide dismutase enzyme activity in the embryonic heart. Maternal dietary organic Mn supplementation effectively eliminated the impairment of maternal environmental hyperthermia on the embryonic development. Maternal dietary manganese supplementation up-regulated manganese superoxide dismutase mRNA expression by reducing DNA methylation and increasing histone 3 lysine 9 acetylation of its promoter. It is suggested that maternal dietary manganese addition could protect the chick embryonic development against maternal heat stress via enhancing epigenetic-activated antioxidant and anti-apoptotic abilities.
Highlights
Maternal heat stress can impair productive performance and induce abnormal development in embryos and death in animals [1, 2]
To address the roles of the maternal dietary inorganic and organic Mn sources in the development of offspring embryos from the heat stressed broiler breeders as well as the deep mechanisms involved, the related data collected from chick embryos delivered from the control broiler breeders in our previous published study [31] were used for statistical analyses in the present study
The previous study [31] was conducted at the same time and facility as this study, and the broiler breeders raised at the normal temperature with a Mn-unsupplemented diet or the basal diet supplemented with the inorganic Mn were treated as the control maternal groups for the present study in accordance with the requirements of the Animal Welfare Committee of the Institute of Animal Science, Chinese Academy of Agricultural Sciences
Summary
Maternal heat stress can impair productive performance and induce abnormal development in embryos and death in animals [1, 2]. Exposure of embryos to oxidative stress can induce DNA damage [4, 5] and increase apoptosis [6], leading to developmental arrest or embryonic death in mammals [4, 7]. The alteration of the epigenetic status was associated with abnormal development and embryo death in vitro [11]. It is speculated that aberrant patterns of DNA methylation and histone acetylation induced by maternal heat stress could cause abnormal embryo development by altering imprinted gene expression using a poultry model
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