Non‐infectious prenatal mortality severely affects the porcine industry, with pathological placentation as a likely key reason. Previous studies have demonstrated that peroxisome proliferator‐activated receptor gamma (PPARγ) deficiency causes defects in the uteroplacental vasculature and induces embryonic losses in mice. However, its role in porcine placental angiogenesis remains unclear. In the present study, PPARγ expression was investigated in porcine uteroplacental tissues at gestational day (GD) 25, GD40 and GD70 via quantitative polymerase chain reaction (qPCR), Western blot and immunohistochemistry (IHC). Moreover, the roles of PPARγ in porcine placental angiogenesis were investigated using a cell model of porcine umbilical vein endothelial cells (PUVECs) to conduct proliferation, migration and tube formation assays in vitro and a mouse xenograft model to assess capillary formation in vivo. The results showed that PPARγ was mainly located in the glandular epithelium, trophoblast, amniotic chorion epithelium and vascular endothelium, as indicated by the higher expression levels at GD25 and GD40 than at GD70 in endometrium and by higher expression levels at GD40 and GD70 than at GD25 in placenta. Moreover, PPARγ expression was significantly downregulated in placenta with dead foetus. In PUVECs, knocking out PPARγ significantly inhibited proliferation, migration and tube formation in vitro and inhibited capillary formation in mouse xenografts in vivo by blocking S‐phase, promoting apoptosis and downregulating the angiogenic factors of VEGF and its receptors. Overall, the spatiotemporal heterogeneity of PPARγ expression in porcine uteroplacental tissue suggests its vital role in endometrial remodelling and placental angiogenesis, and PPARγ regulates placental angiogenesis through VEGF‐mediated signalling.

中文翻译：

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猪子宫内膜中PPARγ表达的时空异质性通过VEGF介导的信号调节胎盘血管生成。

非感染性产前死亡率严重影响猪业，病理性胎盘感染可能是关键原因。先前的研究表明，过氧化物酶体增殖物激活的受体γ（PPARγ）缺乏会引起子宫胎盘血管系统的缺陷，并导致小鼠胚胎丢失。然而，其在猪胎盘血管生成中的作用仍不清楚。在本研究中，通过定量聚合酶链反应（qPCR），蛋白质印迹和免疫组化（IHC）研究了在妊娠第25天（GD），GD40和GD70的猪子宫胎盘组织中PPARγ的表达。此外，使用猪脐静脉内皮细胞（PUVEC）进行增殖的细胞模型研究了PPARγ在猪胎盘血管生成中的作用，体外迁移和管形成测定以及小鼠异种移植模型以评估体内毛细血管形成。结果表明，PPARγ主要位于腺上皮，滋养细胞，羊膜绒毛膜上皮和血管内皮中，其表现为子宫内膜中GD25和GD40的表达水平高于GD70，GD40和GD70的表达水平高于GD25。在胎盘。此外，胎盘已死的胎儿中PPARγ表达显着下调。在PUVEC中，敲除PPARγ可通过阻断S期，促进细胞凋亡并下调VEGF及其受体的血管生成因子，从而在体外显着抑制小鼠异种移植物中的增殖，迁移和管形成，并抑制体内毛细血管形成。总体，