Seminal plasma uterine priming is important for pregnancy and offspring phenotype in mice and swine; however, impacts on the uterus of the dam and her offspring in cattle are unknown. We sought to determine the effects of seminal plasma uterine priming at estrus on uterine transcriptomics, early gestation (d 35, 40, and 45) embryo morphometrics, mid- to late-gestation (d 140 to 220) uterine artery hemodynamics, birth morphometrics, and liver transcriptomics in offspring at 30 d of age. Multiparous Angus-based commercial beef cows were randomly assigned to receive treatment at estrus: 0.5 mL pooled seminal plasma in the uterine body (n = 31, seminal plasma primed) or no treatment (n = 31, control). Seven d later a subset of cows (n = 4/treatment) underwent uterine biopsies, and the remaining cows underwent embryo transfer. Embryo crown-rump length and uterine artery hemodynamics were measured during gestation using ultrasonography. Morphometrics of the calf were collected within 24 h of parturition. Liver biopsies were collected at 30 d of age. Data were analyzed by ANOVA in a completely randomized design for the effect of treatment. Myosin heavy chain I (JSP.1) was downregulated [Benjamin-Hochberg adj P (BH) <= 0.05] and ABO alpha 1-3-N-acetylgalactosaminyltransferase and alpha 1-3-galactosyltransferase (ABO) was upregulated (BH adj P <= 0.05) in the uterus of seminal plasma primed cows 7 d after treatment. Embryo crown-rump length was less (P < 0.05) in seminal plasma primed cows. Mid- to late-gestation (d 140 to 220) uterine artery resistance was increased (P < 0.05) in seminal plasma primed cows. Seminal plasma priming did not alter birth weights or curve-crown-rump length, but heart girth was increased (P < 0.05) in offspring from seminal plasma primed cows. There were no differentially expressed genes (BH adj P <= 0.05) in offspring liver at 30 d of age; however, myosin light chain, phosphorylatable, fast skeletal muscle (MYLPF) was absent in all liver samples from calves from seminal plasma primed cows. In contrast, vomeronasal 1 receptor bosTauV1R414 (BOSTAUV1R414) was present in 6 of the 7 liver samples from calves from seminal plasma primed cows. Seminal plasma uterine priming alters uterine transcriptomics, negatively impacts early gestation embryo growth and mid- to late-gestation uterine artery resistance suggesting downstream vascular anomalies. However, these in utero conditions did not impact offspring from birth to 30 d of age.

中文翻译：

---

精浆子宫启动会改变子宫转录组学，并对肉牛的胚胎生长和子宫动脉抵抗产生负面影响，但不会对后代肝脏转录组学产生负面影响


精浆子宫启动对小鼠和猪的妊娠和后代表型很重要;然而，对母鼠的子宫和她的后代对牛的影响尚不清楚。我们试图确定发情时精浆子宫启动对子宫转录组学、妊娠早期 （d 35、40 和 45） 胚胎形态学、妊娠中晚期 （d 140 至 220） 子宫动脉血流动力学、出生形态学和肝脏转录组学的影响30 d 龄后代。以安格斯为基础的经产商业肉牛被随机分配在发情期接受治疗：子宫体内 0.5 mL 混合精浆（n = 31，精浆启动）或不处理（n = 31，对照）。7 天后，一部分奶牛 （n = 4/治疗） 接受了子宫活检，其余奶牛接受了胚胎移植。妊娠期间使用超声检查测量胚胎冠臀长度和子宫动脉血流动力学。在分娩后 24 小时内收集犊牛的形态测量学。在 30 d 龄时收集肝活检。通过方差分析在完全随机设计中分析治疗效果。肌球蛋白重链 I （JSP.1） 在精浆引发奶牛的子宫中下调 [Benjamin-Hochberg adj P （BH） <= 0.05] 和 ABO α 1-3-N-乙酰半乳糖胺转移酶和 α 1-3-半乳糖基转移酶 （ABO） 上调 （BH 调整 P <= 0.05） 处理 7 d 后。精浆引发奶牛的胚胎冠臀长度较少 （P < 0.05）。精浆启动奶牛妊娠中晚期 （d 140 至 220） 子宫动脉阻力增加 （P < 0.05）。精浆启动不会改变出生体重或曲线-冠-臀部长度，但心围增加（P < 0.05） 在精浆引发奶牛的后代中。30 d 龄后代肝脏无差异表达基因 （BH adj P <= 0.05）;然而，精浆引发奶牛犊牛的所有肝脏样本中均不存在肌球蛋白轻链、磷酸化、快骨骼肌 （MYLPF）。相比之下，犁鼻 1 受体 bosTauV1R414 （BOSTAUV1R414） 存在于精浆引发奶牛犊牛的 7 个肝脏样本中的 6 个中。精浆子宫启动改变了子宫转录组学，对早期妊娠胚胎生长和妊娠中晚期子宫动脉阻力产生负面影响，表明下游血管异常。然而，这些在子宫内的条件不会影响从出生到 30 d 龄的后代。