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RACK1 may participate in placental development at mid-gestation via regulating trophoblast cell proliferation and migration in pigs
Molecular Reproduction and Development ( IF 2.5 ) Pub Date : 2023-03-13 , DOI: 10.1002/mrd.23680
Zhimin Wu 1, 2 , Guangling Hu 1, 2 , Ting Gong 1, 2 , Qun Hu 3 , Linjun Hong 3 , Yiyu Zhang 1, 2 , Zheng Ao 1, 2
Affiliation  

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.

中文翻译:

RACK1 可能通过调节猪的滋养层细胞增殖和迁移参与妊娠中期的胎盘发育

宫内生长受限 (IUGR) 是养猪生产中的严重并发症。胎盘功能不全是胎儿生长不足的原因,但胎盘功能障碍引起的猪 IUGR 的具体病因仍知之甚少。在这项工作中,收集了妊娠第 65 天 (D65) 同窝仔猪中体重最轻 (LW) 和平均体重 (MW) 的胎盘样本,并使用组织形态学研究了胎儿生长与胎盘形态和功能之间的关系LW 和 MW 胎盘中的分析、RNA 测序、定量聚合酶链反应和体外实验。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 (RACK1) 受体的基因在 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,DEGs 主要富集在翻译、核糖体、蛋白质合成和哺乳动物雷帕霉素靶标 (mTOR) 信号通路中。体外实验表明,LW胎盘中降低的RACK1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(PFs)的异常发育。总之,这些结果表明 RACK1 可能通过调节猪的滋养层细胞增殖和迁移而成为 PF 发育的重要调节因子。
更新日期:2023-03-13
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