ArticlePloS one2015
Single administration of ultra-low-dose lipopolysaccharide in rat early pregnancy induces TLR4 activation in the placenta contributing to preeclampsia.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 2 of them syntheses that pooled it.
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Who cites it
51 citing papers in PubMed, 2 syntheses or guidelines pooled it, 96 citations in OpenAlex.
- Guidelines for assessing maternal cardiovascular physiology during pregnancy and postpartum.American journal of physiology. Heart and circulatory physiology · 2024Guideline
- Association Between TLR4 Gene Polymorphisms and Risk of Preeclampsia: Systematic Review and Meta-Analysis.Medical science monitor : international medical journal of experimental and clinical research · 2021Pooled it
- Agomelatine ameliorates abortion-related alterations in rats: Insights from behavioural, biochemical and histological analyses.Experimental physiology · 2026Article
- Decoding preeclampsia: A fusion of multi-view machine learning and multi-omics to identify putative inflammation-related mechanisms.Molecular therapy. Nucleic acids · 2026Article
- LAMB1 regulates COL3A1 and RAC1 expression during subchorionic hemorrhage progression.BMC biology · 2026Article
- Pyridostigmine Attenuated Placental Ischemia-Upregulated Paraventricular Nucleus TLR4-Associated Hypertension in Preeclamptic Rats.Molecular neurobiology · 2026Article
- NFĸB and its inhibitors in preeclampsia: mechanisms and potential interventions.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- N,N-Diethylacetamide and N,N-Dipropylacetamide inhibit the NF-kB pathway in in vitro, ex vivo and in vivo models of inflammation-induced preterm birth.Scientific reports · 2025Article
- Mannose-B from Codonopsis pilosula modulates LAMB1 expression to enhance trophoblast function and alleviate subchorionic hematoma.Scientific reports · 2025Article
- Decreased PD-L1 contributes to preeclampsia by suppressing GM-CSF via the JAK2/STAT5 signal pathway.Scientific reports · 2025Article
- Gestationally administered RAS modulators reprogram endotoxic cardiovascular and inflammatory profiles in adult male offspring of preeclamptic rats.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Immune dysregulation in preeclampsia: integrative analysis of peripheral transcriptomes and placental single-cell land-scapes.Frontiers in immunology · 2025Article
- Distinct phenotypes in the preeclamptic-like mouse model induced by adenovirus carrying sFlt1 and recombinant sFlt1 protein.European journal of medical research · 2024Article
- Cited2 is a key regulator of placental development and plasticity.BioEssays : news and reviews in molecular, cellular and developmental biology · 2024Review
- The NFκB Signaling Pathway Is Involved in the Pathophysiological Process of Preeclampsia.Geburtshilfe und Frauenheilkunde · 2024Article
- The Role of Catestatin in Preeclampsia.International journal of molecular sciences · 2024Review
- Maternal immune activation and role of placenta in the prenatal programming of neurodevelopmental disorders.Neuronal signaling · 2023Review
- 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
- Article
- A comparison of rat models that best mimic immune-driven preeclampsia in humans.Frontiers in endocrinology · 2023Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Balanced immune responses are essential for the maintenance of successful pregnancy. Aberrant responses of immune system during pregnancy increase the risk of preeclampsia. Toll-like receptor 4 (TLR4) plays a crucial role in the activation of immune system at the maternal-fetal interface. This study aimed to generate a rat model of preeclampsia by lipopolysaccharide (LPS, a TLR4 agonist) administration on gestational day (GD) 5 as rats are subjected to placentation immediately after implantation between GDs 4 and 5, and to assess the contribution of TLR4 signaling to the development of preeclampsia. Single administration of 0.5 μg/kg LPS significantly increased blood pressure of pregnant rats since GD 6 (systolic blood pressure, 124.89 ± 1.79 mmHg versus 119.02 ± 1.80 mmHg, P < 0.05) and urinary protein level since GD 9 (2.02 ± 0.29 mg versus 1.11 ± 0.18 mg, P < 0.01), but barely affected blood pressure or proteinuria of virgin rats compared with those of saline-treated pregnant rats. This was accompanied with adverse pregnancy outcomes including fetal growth restriction. The expression of TLR4 and NF-κB p65 were both increased in the placenta but not the kidney from LPS-treated pregnant rats, with deficient trophoblast invasion and spiral artery remodeling. Furthermore, the levels of inflammatory cytokines were elevated systemically and locally in the placenta from pregnant rats treated with LPS. TLR4 signaling in the placenta was activated, to which that in the placenta of humans with preeclampsia changed similarly. In conclusion, LPS administration to pregnant rats in early pregnancy could elicit TLR4-mediated immune response at the maternal-fetal interface contributing to poor early placentation that may culminate in the preeclampsia-like syndrome.
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