ArticleThe American journal of pathology2009
Characterization of RAGE, HMGB1, and S100beta in inflammation-induced preterm birth and fetal tissue injury.
Article in The American journal of pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 84 citations in OpenAlex.
- Assessment of DHA on reducing early preterm birth: the ADORE randomized controlled trial protocol.BMC pregnancy and childbirth · 2017Trial
- RAGE controls leukocyte adhesion in preterm and term infants.BMC immunology · 2014Trial
- RAGE-Mediated Signalling in Gynaecological Disorders: Review of Molecular Mechanisms and Therapeutic Perspectives.Expert reviews in molecular medicine · 2026Review
- Article
- Predictors of Inflammation-Mediated Preterm Birth.Physiology (Bethesda, Md.) · 2025Review
- Inflammatory mediators and the RAGE pathway in placental tissues of pregnancies complicated by severe preeclampsia.Frontiers in reproductive health · 2025Article
- Stretch Causes cffDNA and HMGB1-Mediated Inflammation and Cellular Stress in Human Fetal Membranes.International journal of molecular sciences · 2024Article
- Is human labor at term an inflammatory condition?†.Biology of reproduction · 2023Review
- RAGE against the Machine: Can Increasing Our Understanding of RAGE Help Us to Battle SARS-CoV-2 Infection in Pregnancy?International journal of molecular sciences · 2022Review
- Sitagliptin attenuates arterial calcification by downregulating oxidative stress-induced receptor for advanced glycation end products in LDLR knockout mice.Scientific reports · 2021Article
- Higher dose docosahexaenoic acid supplementation during pregnancy and early preterm birth: A randomised, double-blind, adaptive-design superiority trial.EClinicalMedicine · 2021Article
- Extracellular vesicle mediated feto-maternal HMGB1 signaling induces preterm birth.Lab on a chip · 2021Article
- High-mobility group box 1 is a driver of inflammation throughout pregnancy.American journal of reproductive immunology (New York, N.Y. : 1989) · 2021Review
- Biomarker Potential of the Soluble Receptor for Advanced Glycation End Products to Predict Bronchopulmonary Dysplasia in Premature Newborns.Frontiers in pediatrics · 2021Article
- Novel pathways of inflammation in human fetal membranes associated with preterm birth and preterm pre-labor rupture of the membranes.Seminars in immunopathology · 2020Review
- Targeting Toll-like receptor-4 to tackle preterm birth and fetal inflammatory injury.Clinical & translational immunology · 2020Review
- Differential expression and role of S100 proteins in chronic rhinosinusitis.Current opinion in allergy and clinical immunology · 2020Review
- Microglia Susceptibility to Free Bilirubin Is Age-Dependent.Frontiers in pharmacology · 2020Article
- Initiation of human parturition: signaling from senescent fetal tissues via extracellular vesicle mediated paracrine mechanism.Obstetrics & gynecology science · 2019Review
- The role of Th17 cells in the pathophysiology of pregnancy and perinatal mood and anxiety disorders.Brain, behavior, and immunity · 2019Review
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
Immune activation represents an adaptive reaction triggered by both noxious exogenous (microbes) and endogenous [high mobility group box-1 protein (HMGB1), S100 calcium binding proteins] inducers of inflammation. Cell stress or necrosis lead the release of HMGB1 and S100 proteins in the extracellular compartment where they act as damage-associated molecular pattern molecules (or alarmins) by engaging the receptor for advanced glycation end-products (RAGE). Although the biology of RAGE is dictated by the accumulation of damage-associated molecular pattern molecules at sites of tissue injury, the role of RAGE in mediating antenatal fetal injury remains unknown. First, we studied the relationships at birth between the intensity of human fetal inflammation and sRAGE (an endogenous RAGE antagonist), HMGB1, and S100beta protein. We found significantly lower sRAGE in human fetuses that mounted robust inflammatory responses. HMGB1 levels correlated significantly with levels of interleukin-6 and S100beta in fetal circulation. We then evaluated the levels and areas of tissue expression of RAGE, HMGB1, and S100beta in specific organs of mouse fetuses on E16. Using an animal model of endotoxin-induced fetal damage and preterm birth, we determined that inflammation induces a significant change in expression of RAGE and HMGB1, but not S100beta, at sites of tissue damage. Our findings indicate that RAGE and HMGB1 may be important mediators of cellular injury in fetuses delivered in the setting of inflammation-induced preterm birth.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.