ArticleAmerican journal of obstetrics and gynecology2009
Beyond white matter damage: fetal neuronal injury in a mouse model of preterm birth.
Article in American journal of obstetrics and gynecology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
41 citing papers in PubMed, 62 citations in OpenAlex.
- Preterm birth: A neuroinflammatory origin for metabolic diseases?Brain, behavior, & immunity - health · 2024Review
- Intrauterine colonization with Gardnerella vaginalis and Mobiluncus mulieris induces maternal inflammation but not preterm birth in a mouse model.American journal of reproductive immunology (New York, N.Y. : 1989) · 2023Article
- Intra-amniotic inflammation in the mid-trimester of pregnancy is a risk factor for neuropsychological disorders in childhood.Journal of perinatal medicine · 2023Article
- Editorial: Advances and perspectives in neuroplacentology.Frontiers in endocrinology · 2023Article
- RAC1 is involved in uterine myometrium contraction in the inflammation-associated preterm birth.Reproduction (Cambridge, England) · 2022Article
- Review
- Next generation strategies for preventing preterm birth.Advanced drug delivery reviews · 2021Review
- IFNγ-Producing γ/δ T Cells Accumulate in the Fetal Brain Following Intrauterine Inflammation.Frontiers in immunology · 2021Article
- The role of in utero endotoxin exposure in the development of inflammatory bowel disease in mice.American journal of reproductive immunology (New York, N.Y. : 1989) · 2020Article
- Dose-dependent structural and immunological changes in the placenta and fetal brain in response to systemic inflammation during pregnancy.American journal of reproductive immunology (New York, N.Y. : 1989) · 2020Article
- Characterization of an Adapted Murine Model of Intrauterine Inflammation-Induced Preterm Birth.The American journal of pathology · 2020Article
- Herpesvirus-infected Hofbauer cells activate endothelial cells through an IL-1β-dependent mechanism.Placenta · 2020Article
- The orphan nuclear receptor Nr4a1 mediates perinatal neuroinflammation in a murine model of preterm labor.Cell death & disease · 2020Article
- The tracking of lipopolysaccharide through the feto-maternal compartment and the involvement of maternal TLR4 in inflammation-induced fetal brain injury.American journal of reproductive immunology (New York, N.Y. : 1989) · 2019Article
- The Absence of TLR4 Prevents Fetal Brain Injury in the Setting of Intrauterine Inflammation.Reproductive sciences (Thousand Oaks, Calif.) · 2019Article
- Maternal Supplementation of Low Dose Fluoride Alleviates Adverse Perinatal Outcomes Following Exposure to Intrauterine Inflammation.Scientific reports · 2019Article
- Maternal CD8American journal of reproductive immunology (New York, N.Y. : 1989) · 2018Article
- In vivo assessment of the placental anatomy and perfusion in a mouse model of intrauterine inflammation.Journal of magnetic resonance imaging : JMRI · 2018Article
- Long-term impact of intrauterine neuroinflammation and treatment with magnesium sulphate and betamethasone: Sex-specific differences in a preterm labor murine model.Scientific reports · 2017Article
- Maternal dendrimer-based therapy for inflammation-induced preterm birth and perinatal brain injury.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
objectiveThe purpose of this study was to elucidate possible mechanisms of fetal neuronal injury in inflammation-induced preterm birth. STUDY
designWith the use of a mouse model of preterm birth, the following primary cultures were prepared from fetal brains: (1) control neurons (CNs), (2) lipopolysaccharide-exposed neurons (LNs), (3) control coculture (CCC) that consisted of neurons and glia, and (4) lipopolysaccharide-exposed coculture (LCC) that consisted of lipopolysaccharide-exposed neurons and glia. CNs and LNs were treated with culture media from CN, LN, CCC, and LCC after 24 hours in vitro. Immunocytochemistry was performed for culture characterization and neuronal morphologic evidence. Quantitative polymerase chain reaction was performed for neuronal differentiation marker, microtubule-associated protein 2, and for cell death mediators, caspases 1, 3, and 9.
resultsLipopolysaccharide exposure in vivo did not influence neuronal or glial content in cocultures but decreased the expression of microtubule-associated protein 2 in LNs. Media from LNs and LCCs induced morphologic changes in control neurons that were comparable with LNs. The neuronal damage caused by in vivo exposure (LNs) could not be reversed by media from control groups.
conclusionLipopolysaccharide-induced preterm birth may be responsible for irreversible neuronal injury.
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