Abstract

Abstract Vitamins and minerals are essential for proper fetal and placental development and function. However, the impact of micronutrient supplementation on placental function and gene expression remains unclear. Herein, we performed a transcriptomic analysis to determine the impact of pre-breeding maternal micronutrient supplementation on the gene expression of placental caruncles (CAR; maternal placenta). Crossbred Angus beef heifers were supplemented (VTM, n = 7) or not (CON, n = 7) with 113 g•heifer-1•d-1 of mineral premix (Purina® Wind & Rain® Storm® All-Season 7.5 Complete) from d 71 to 148 before breeding and until d 83 of gestation. After breeding, heifers were fed a diet to gain 0.79 kg/d. Uteroplacental tissues were collected at d 83. The largest placentome closest to the fetus was collected, and CAR was manually dissected from the cotyledon. Total RNA was isolated from CAR, and gene expression was measured with RNA-Seq. After data quality control and read mapping, differential expression was performed using DESeq2. We identified 46 upregulated and 19 downregulated genes in the VTM group (adj.Pval < 0.1). ShinyGO pathway analysis software was used to identify genes in the Ca and CGMP-PKG signaling pathways, including CALM2 and CAMK2G, which were down and upregulated, respectively. Calcium-mediated systems may activate steroidogenic activity in bovine placentomes, while the cGMP-PKG pathway plays a key role in vascular homeostasis mediated by nitric oxide and decreased Ca concentrations. Furthermore, biological processes underlying blood circulation were among those over-represented. Previous studies report that maternal nutrition may impact placental vascularity and uterine blood flow. ATP2B, that is upregulated in the VTM group, is a calcium/calmodulin-regulated, magnesium-dependent protein involved in intracellular Ca homeostasis. In summary, pre-breeding and early gestation maternal micronutrient supplementation leads to differential expression of genes involved in Ca homeostasis and has a putative effect on placenta vascular function.

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