PSG1 in Regulating Proliferation and Migration of Human Umbilical Vein Endothelial Cells Through the TGF-β/Orai3 Signaling Pathway

IF 1.5 4区医学 Q3 OBSTETRICS & GYNECOLOGY

Journal of Obstetrics and Gynaecology Research Pub Date : 2025-10-09 DOI:10.1111/jog.70092

Yali Yang, Qiaofang Yang, Shanyan Lai, Mianbo Lin, Lichao Yuan, Guilan Nie, Xufei Fan

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引用次数: 0

Abstract

Purpose

To study the function of pregnancy-specific glycoprotein 1 (PSG1) in regulating proliferation, migration, and vascular tone of human umbilical vein endothelial cells (HUVECs), and further explore its role in placental development and potential molecular mechanisms through co-culturing HUVECs with HTR8/svneo cells.

Methods

HUVECs were treated with 2, 4, and 8 μg/mL PSG1. The Cell Counting Kit-8 assay was used to test cell proliferation, apoptosis by Annexin V/PI staining, and intracellular calcium and nitric oxide (NO) levels by fluorescence microscopy. Western blotting quantified the expression of vascular endothelial growth factor (VEGF), transforming growth factor-beta (TGF-β), endothelial nitric oxide synthase (eNOS), calcium release-activated calcium channel protein 3 (Orai3), and PSG1. To study PSG1's effect on placental development, HUVECs were co-cultured with HTR8/svneo cells. siRNA-mediated knockdown of PSG1 was performed in both cell types to evaluate its impact on endothelial function, vascular tone, and trophoblast-endothelial cell interactions.

Results

PSG1 treatment enhanced HUVEC proliferation, with high concentrations reducing apoptosis. PSG1 upregulated the expression of VEGF, TGF-β, eNOS, and Orai3, and significantly increased both intracellular calcium and NO levels. Knockdown of PSG1 reduced these effects in HUVECs, and co-culture with PSG1-deficient trophoblast cells further diminished HUVEC proliferation, enhanced apoptosis, and decreased NO release. Our study highlighted the crucial role of PSG1 in endothelial cell function and vascular tone regulation. Furthermore, PSG1 modulation influenced eNOS activity, enhancing NO release, which contributed to vascular dilation.

Conclusions

PSG1 promotes HUVEC proliferation, inhibits apoptosis, and regulates vascular tone through the TGF-β/Orai3 signaling pathway, primarily by modulating NO production.

查看原文本刊更多论文

PSG1通过TGF-β/Orai3信号通路调控人脐静脉内皮细胞增殖和迁移

目的：研究妊娠特异性糖蛋白1 （PSG1）在调节人脐静脉内皮细胞（HUVECs）增殖、迁移和血管张力中的功能，并通过与HTR8/svneo细胞共培养进一步探讨其在胎盘发育中的作用及其可能的分子机制。方法：分别用2、4、8 μg/mL的PSG1治疗HUVECs。细胞计数试剂盒-8检测细胞增殖，Annexin V/PI染色检测细胞凋亡，荧光显微镜检测细胞内钙和一氧化氮（NO）水平。Western blotting定量检测血管内皮生长因子（VEGF）、转化生长因子-β (TGF-β)、内皮型一氧化氮合酶（eNOS）、钙释放激活钙通道蛋白3 （Orai3）、PSG1的表达。为了研究PSG1对胎盘发育的影响，我们将HUVECs与HTR8/svneo细胞共培养。在两种细胞类型中进行了sirna介导的PSG1敲低，以评估其对内皮功能、血管张力和滋养细胞与内皮细胞相互作用的影响。结果：PSG1可增强HUVEC增殖，高浓度可减少凋亡。PSG1上调VEGF、TGF-β、eNOS和Orai3的表达，显著升高细胞内钙和NO水平。敲低PSG1可降低HUVEC的这些作用，与PSG1缺失的滋养细胞共培养进一步降低HUVEC的增殖，增强凋亡，减少NO的释放。我们的研究强调了PSG1在内皮细胞功能和血管张力调节中的关键作用。此外，PSG1调节影响eNOS活性，增加NO释放，促进血管扩张。结论：PSG1通过TGF-β/Orai3信号通路促进HUVEC增殖，抑制凋亡，调节血管张力，主要通过调节NO的产生。

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来源期刊

Journal of Obstetrics and Gynaecology Research 医学-妇产科学

CiteScore

3.10

自引率

0.00%

发文量

376

审稿时长

3-6 weeks

期刊介绍： The Journal of Obstetrics and Gynaecology Research is the official Journal of the Asia and Oceania Federation of Obstetrics and Gynecology and of the Japan Society of Obstetrics and Gynecology, and aims to provide a medium for the publication of articles in the fields of obstetrics and gynecology. The Journal publishes original research articles, case reports, review articles and letters to the editor. The Journal will give publication priority to original research articles over case reports. Accepted papers become the exclusive licence of the Journal. Manuscripts are peer reviewed by at least two referees and/or Associate Editors expert in the field of the submitted paper.