ArticleProceedings of the National Academy of Sciences of the United States of America2017
Up-regulation of CD81 inhibits cytotrophoblast invasion and mediates maternal endothelial cell dysfunction in preeclampsia.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 52 citations in OpenAlex.
- CD81 restricts decidual IGF2-mediated smooth muscle cell dedifferentiation during spiral artery remodeling in preeclampsia.BMC medicine · 2026Article
- Rational Design of Nanomedicine for Placental Disorders: Birthing a New Era in Women's Reproductive Health.Small (Weinheim an der Bergstrasse, Germany) · 2024Review
- Single-cell and spatial transcriptomics reveal alterations in trophoblasts at invasion sites and disturbed myometrial immune microenvironment in placenta accreta spectrum disorders.Biomarker research · 2024Article
- Circulating extracellular vesicles and neutrophil extracellular traps contribute to endothelial dysfunction in preeclampsia.Frontiers in immunology · 2024Article
- IFITM1 inhibits trophoblast invasion and is induced in placentas associated with IFN-mediated pregnancy diseases.iScience · 2023Article
- Renal CD81 interacts with sodium potassium 2 chloride cotransporter and sodium chloride cotransporter in rats with lipopolysaccharide-induced preeclampsia.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- Increased Expression of Tetraspanins, ALIX and HSP-70 in the Placenta Tissue of Women with Chronic Venous Disease during Pregnancy.International journal of medical sciences · 2023Article
- Article
- Serum from patients with hypertension promotes endothelial dysfunction to induce trophoblast invasion through the miR‑27b‑3p/ATPase plasma membrane CaMolecular medicine reports · 2021Article
- The potential role of pregnancy-associated plasma protein-A2 in angiogenesis and development of preeclampsia.Hypertension research : official journal of the Japanese Society of Hypertension · 2019Article
- Upregulation of CD81 in trophoblasts induces an imbalance of Treg/Th17 cells by promoting IL-6 expression in preeclampsia.Cellular & molecular immunology · 2019Article
- Pravastatin alleviates lipopolysaccharide-induced placental TLR4 over-activation and promotes uterine arteriole remodeling without impairing rat fetal development.Journal of biomedical research · 2018Article
Corrections and comments
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Authors and funding
16 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Preeclampsia (PE) is initiated by abnormal placentation in the early stages of pregnancy, followed by systemic activation of endothelial cells of the maternal small arterioles in the late second or third trimester (TM) of pregnancy. During normal pregnancy, placental cytotrophoblasts (CTBs) invade the maternal uterine wall and spiral arteries, whereas this process is interrupted in PE. However, it is not known how the malformed placenta triggers maternal endothelial crisis and the associated manifestations. Here, we have focused on the association of CD81 with PE. CD81, a member of the tetraspanin superfamily, plays significant roles in cell growth, adhesion, and motility. The function of CD81 in human placentation and its association with pregnancy complications are currently unknown. In the present study, we have demonstrated that CD81 was preferentially expressed in normal first TM placentas and progressively down-regulated with gestation advance. In patients with early-onset severe PE (sPE), CD81 expression was significantly up-regulated in syncytiotrophoblasts (STBs), CTBs and the cells in the villous core. In addition, high levels of CD81 were observed in the maternal sera of patients with sPE. Overexpressing CD81 in CTBs significantly decreased CTB invasion, and culturing primary human umbilical vein endothelial cells (HUVECs) in the presence of a high dose of exogenous CD81 resulted in interrupted angiogenesis and endothelial cell activation in vitro. Importantly, the phenotype of human PE was mimicked in the CD81-induced rat model.
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