ArticleExperimental and therapeutic medicine2021
Increased expression of IFN-γ in preeclampsia impairs human trophoblast invasion via a SOCS1/JAK/STAT1 feedback loop.
Article in Experimental and therapeutic medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 33 citations in OpenAlex.
- Calcifediol Suppressed Placental Inflammation and Improved Pregnancy Outcomes by Targeting JAK/STAT Signaling Pathway in Preeclampsia.American journal of reproductive immunology (New York, N.Y. : 1989) · 2026Article
- TLR7 alters the maternal immune landscape during influenza A infection to increase maternal and fetal morbidity.Science advances · 2026Article
- IFN-γ+ NK cells as a potential predictor of pregnancy loss in unexplained recurrent pregnancy loss.International journal of medical sciences · 2026Article
- SOCS1 improves abnormal IgA galactosylation in IgA nephropathy by regulating the TLR9/MyD88 pathway.Immunologic research · 2025Article
- Role of HMGB1 on the onset of preeclampsia.BMC pregnancy and childbirth · 2025Article
- Nutraceuticals as Modulators of Molecular Placental Pathways: Their Potential to Prevent and Support the Treatment of Preeclampsia.International journal of molecular sciences · 2024Review
- Exploring the ceRNA network involving AGAP2-AS1 as a novel biomarker for preeclampsia.Scientific reports · 2024Article
- Biomarkers and point of care screening approaches for the management of preeclampsia.Communications medicine · 2024Review
- Effect of Granzyme K, FasL and Interferon-γ Expression in Placentas with Preeclampsia.Biomedicines · 2024Article
- Article
- A loss of function mutation in SOCS2 results in increased inflammatory response of macrophages to TLR ligands andFrontiers in immunology · 2024Article
- Deciphering the immunological interactions: targeting preeclampsia with Hydroxychloroquine's biological mechanisms.Frontiers in pharmacology · 2024Review
- The Role of Interferon (IFN)-γ in Extravillous Trophoblast Cell (EVT) Invasion and Preeclampsia Progression.Reproductive sciences (Thousand Oaks, Calif.) · 2023Review
- Preeclampsia Susceptibility Assessment Based on Deep Learning Modeling and Single Nucleotide Polymorphism Analysis.Biomedicines · 2023Article
- Chromogranin A: An Endocrine Factor of Pregnancy.International journal of molecular sciences · 2023Review
- Exploring the role of T helper subgroups and their cytokines in the development of pregnancy-induced hypertension.Frontiers in immunology · 2023Article
- Down-regulation of microRNA-155 suppressed Candida albicans induced acute lung injury by activating SOCS1 and inhibiting inflammation response.Journal of microbiology (Seoul, Korea) · 2022Article
- Pro- and Anti-Inflammatory Cytokines in the Context of NK Cell-Trophoblast Interactions.International journal of molecular sciences · 2022Article
- FABP4 activates the JAK2/STAT2 pathway via Rap1a in the homocysteine-induced macrophage inflammatory response in ApoELaboratory investigation; a journal of technical methods and pathology · 2022Article
- IFN-γ inhibits ovarian cancer progression via SOCS1/JAK/STAT signaling pathway.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022Article
Corrections and comments
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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
The weakening of extravillous trophoblast (EVT) invasion results in shallow placenta implantation. In HTR8/SVneo cells, IFN-γ can activate STAT1 and reduce cell invasion, and suppressor of cytokine signaling (SOCS) is an important negative regulatory protein in the Janus kinase (JAK)/STAT activator pathway and has a negative feedback function on JAK/STAT1. The aim of the present study was to elucidate how SOCS1 feedback regulates JAK/STAT1 and affects EVT cell invasion, which in turn affects the development of preeclampsia (PE). MTT and Annexin V/phosphatidylserine (PS) assays were performed to evaluate the viability and apoptosis of HTR8/SVneo cells treated with IFN-γ, respectively. Wound healing and invasion assays were also conducted to measure the migratory and invasive abilities of IFN-γ-treated HTR8/SVneo cells. The mRNA and protein expression levels of genes were detected using reverse transcription-quantitative PCR and western blot analysis. Small interfering RNA knockdown of SOCS1 was used to verify the role of feedback regulation in the IFN-γ-activated JAK/STAT1 signaling pathway. IFN-γ can inhibit HTR8/SVneo migration and invasion, and promote apoptosis by increasing the expression of phosphorylated (p)-JAK, p-STAT1 and caspase3, and reducing the expression of platelet-derived growth factor receptor A and Ezrin. Furthermore, SOCS1 may negatively regulate JAK/STAT1 and affect HTR-8/SVneo invasiveness. Evaluation of clinical samples demonstrated that the expression levels of SOCS1 and IFN-γ were higher in patients with PE compared with the healthy group. Collectively, the present results indicated that IFN-γ reduced the invasion of HTR-8/SVneo cells by activating JAK/STAT1, concurrently leading to an increase in SOCS1, which negatively regulates JAK/STAT1 and eliminates the pro-inflammatory effects of IFN-γ, thus forming a feedback loop.
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