Department of Bioproduction, Graduate School of Bioindustry, Tokyo University of Agriculture, Abashiri, Hokkaido 099-2493, Japan.
NODAI Genome Research Center, Tokyo University of Agriculture, Tokyo 156-8502, Japan.
J Reprod Dev. 2022 Feb 18;68(1):30-37. doi: 10.1262/jrd.2021-094. Epub 2021 Oct 31.
Although hormonal induction of parturition in cattle results in the successful delivery of healthy calves, the risk of retained fetal membrane is significantly increased. In a previous study, a combination of the long-acting glucocorticoid, triamcinolone acetonide, with a high dose of betamethasone partially normalized the placentomal gene expression during parturition; however, the incidence of retained fetal membrane remained high. This study further explored placentomal dysfunction and aimed to elucidate the mechanism of retained fetal membrane in parturition-induced cows. In this study, transcriptome analysis revealed that enhanced glucocorticoid exposure normalized the expression of a substantial fraction of genes in the cotyledons. In contrast, a significant reduction in the multiple signaling pathway activities, including interferon signaling, was found in the caruncles during induced parturition. Real-time PCR showed that the expression of interferon-tau in the caruncles, but not interferon-alpha or interferon-gamma, was significantly lower in induced parturition than spontaneous parturition. Interferon-stimulated gene expression was also significantly decreased in the caruncles during induced parturition. These results indicate that interferon signaling could be important for immunological control in placentomes during parturition. Additionally, this suggests that interferon-tau might be a pivotal ligand for interferon receptors in the caruncles. This study revealed that peripheral blood leukocytes in prepartum cows transcribed interferon-tau. Macrophage infiltration in the placentome is known to participate in the detachment of the fetal membrane from the caruncle. Thus, this study raised the possibility that immune cells migrating into the caruncles at parturition may act as a source of ligands that activate interferon signaling.
虽然激素诱导牛分娩可以成功产下健康的小牛，但胎衣滞留的风险显著增加。在之前的研究中，长效糖皮质激素曲安奈德与高剂量倍他米松联合使用，部分恢复了分娩时胎盘基因的正常表达；然而，胎衣滞留的发生率仍然很高。本研究进一步探讨了胎盘功能障碍，并旨在阐明诱导分娩牛胎衣滞留的机制。在这项研究中，转录组分析显示，增强的糖皮质激素暴露使胎盘中很大一部分基因的表达正常化。相比之下，在诱导分娩期间，多个信号通路的活性显著降低，包括干扰素信号通路。实时 PCR 显示，在诱导分娩中，胎衣中干扰素 - tau 的表达明显低于自然分娩，而干扰素 -α或干扰素 -γ的表达则没有明显降低。在诱导分娩期间，胎盘中干扰素刺激基因的表达也显著降低。这些结果表明，干扰素信号通路在分娩时胎盘的免疫控制中可能很重要。此外，这表明干扰素 -tau 可能是胎盘中干扰素受体的关键配体。本研究表明，产前奶牛的外周血白细胞转录干扰素 -tau。已知胎盘中的巨噬细胞浸润参与了胎衣从胎衣上的分离。因此，本研究提出了一种可能性，即分娩时迁移到胎衣中的免疫细胞可能是激活干扰素信号的配体的来源。
