Wu Zhimin, Hu Guangling, Gong Ting, Hu Qun, Hong Linjun, Zhang Yiyu, Ao Zheng
Key Laboratory of Animal Genetics, Breeding and Reproduction in the Plateau Mountainous Region, Ministry of Education, College of Animal Science, Guizhou University, Guiyang, China.
Guizhou Provincial Key Laboratory of Animal Genetics, Breeding and Reproduction, College of Animal Science, Guizhou University, Guiyang, China.
Mol Reprod Dev. 2023 Apr;90(4):248-259. doi: 10.1002/mrd.23680. Epub 2023 Mar 13.
Intrauterine growth restriction (IUGR) is a severe complication in swine production. Placental insufficiency is responsible for inadequate fetal growth, but the specific etiology of placental dysfunction-induced IUGR in pigs remains poorly understood. In this work, placenta samples supplying the lightest weight (LW) and mean weight (MW) pig fetuses in the litter at Day 65 (D65) of gestation were collected, and the relationship between fetal growth and placental morphologies and functions was investigated using histomorphological analysis, RNA sequencing, quantitative polymerase chain reaction, and in vitro experiment in LW and MW placentas. Results showed that the folded structure of the epithelial bilayer of LW placentas followed a poor and incomplete development compared with that of MW placentas. A total of 654 differentially expressed genes (DEGs) were screened out between the LW and MW placentas, and the gene encodes receptor for activated C kinase 1 (RACK1) was found to be downregulated in LW placentas. The DEGs were mainly enriched in translation, ribosome, protein synthesis, and mammalian target of rapamycin (mTOR) signaling pathway according to gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. In vitro experiments indicated that the decreased RACK1 in LW placentas may be involved in abnormal development of placental folds (PFs) by inhibiting the proliferation and migration of porcine trophoblast cells. Taken together, these results revealed that RACK1 may be a vital regulator in the development of PFs via regulating trophoblast cell proliferation and migration in pigs.
宫内生长受限（IUGR）是养猪生产中的一种严重并发症。胎盘功能不全导致胎儿生长不足，但猪中胎盘功能障碍引起的IUGR的具体病因仍知之甚少。在这项研究中，收集了妊娠65天（D65）时窝中最轻体重（LW）和平均体重（MW）猪胎儿的胎盘样本，并通过组织形态学分析、RNA测序、定量聚合酶链反应以及LW和MW胎盘的体外实验研究了胎儿生长与胎盘形态和功能之间的关系。结果表明，与MW胎盘相比，LW胎盘上皮双层的折叠结构发育不良且不完整。在LW和MW胎盘之间共筛选出654个差异表达基因（DEG），发现编码活化C激酶1受体（RACK1）的基因在LW胎盘中下调。根据基因本体论（GO）和京都基因与基因组百科全书（KEGG）富集分析，DEG主要富集在翻译、核糖体、蛋白质合成和雷帕霉素哺乳动物靶标（mTOR）信号通路中。体外实验表明，LW胎盘中RACK1的减少可能通过抑制猪滋养层细胞的增殖和迁移而参与胎盘褶皱（PF）的异常发育。综上所述，这些结果表明RACK1可能通过调节猪滋养层细胞的增殖和迁移而成为PF发育中的重要调节因子。
