ArticleScientific reports2019
HtrA4 may play a major role in inhibiting endothelial repair in pregnancy complication preeclampsia.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 28 citations in OpenAlex.
- Proteomic Epithelial-To-Mesenchymal Transition Signature in Fetoplacental Small Extracellular Vesicles of Early-Onset Preeclampsia.Journal of extracellular biology · 2026Article
- Htra4 promotes vascular endothelial cell injury and is associated with the early-onset of preeclampsia.Scientific reports · 2025Article
- Identification of critical biomarkers and immune infiltration in preeclampsia through bioinformatics and machine learning methods.BMC pregnancy and childbirth · 2025Article
- Culture of cryopreserved first trimester placental tissues to study syncytial renewal.Scientific reports · 2025Article
- Prevention and treatment of peri-implant fibrosis by functionally inhibiting skeletal cells expressing the leptin receptor.Nature biomedical engineering · 2024Article
- Identification and validation of feature genes associated with M1 macrophages in preeclampsia.Aging · 2023Article
- Endothelial progenitor cells in pregnancy-related diseases.Clinical science (London, England : 1979) · 2023Review
- Article
- A cross-sectional analysis of syncytiotrophoblast membrane extracellular vesicles-derived transcriptomic biomarkers in early-onset preeclampsia.Frontiers in cardiovascular medicine · 2023Article
- Overview of Human HtrA Family Proteases and Their Distinctive Physiological Roles and Unique Involvement in Diseases, Especially Cancer and Pregnancy Complications.International journal of molecular sciences · 2021Review
- HtrA4 is up-regulated during trophoblast syncytialization and BeWo cells fail to syncytialize without HtrA4.Scientific reports · 2021Article
- Alpha-1 Antitrypsin-Induced Endoplasmic Reticulum Stress Promotes Invasion by Extravillous Trophoblasts.International journal of molecular sciences · 2021Article
- Transcriptomic modifications in developmental cardiopulmonary adaptations to chronic hypoxia using a murine model of simulated high-altitude exposure.American journal of physiology. Lung cellular and molecular physiology · 2020Article
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Preeclampsia (PE) is a life-threatening complication of human pregnancy with no effective treatment other than premature delivery. It is hallmarked by systemic endothelial injury/dysfunction which is believed to be caused by abnormal levels/types of placenta-derived factors that are circulating in the maternal blood. Emerging evidence suggests that endothelial repair is also dysregulated in PE, as circulating endothelial progenitor cells (EPCs) critical for endothelial regeneration are reduced in number and functionality. However, the underlying mechanisms are poorly understood. HtrA4 is a placenta-specific protease that is secreted into the circulation and significantly elevated in early-onset PE. Here we investigated the impact of HtrA4 on endothelial proliferation and repair. We demonstrated that high levels of HtrA4 halted endothelial cell proliferation and significantly down-regulated a number of genes that are critical for cell cycle progression, including CDKN3, BIRC5, CDK1 and MKI67. Furthermore, HtrA4 significantly inhibited the proliferation of primary EPCs isolated from term human umbilical cord blood and impeded their differentiation into mature endothelial cells. Our data thus suggests that elevated levels of HtrA4 in the early-onset PE circulation may impair endothelial cell repair, not only by halting endothelial cell proliferation, but also by inhibiting the proliferation and differentiation of circulating EPCs.
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