ArticleReproductive sciences (Thousand Oaks, Calif.)2016
Damage-Associated Molecular Pattern and Fetal Membrane Vascular Injury and Collagen Disorganization in Lipopolysaccharide-Induced Intra-amniotic Inflammation in Fetal Sheep.
Article in Reproductive sciences (Thousand Oaks, Calif.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- Interleukin-1 Receptor Antagonists Partially Inhibited Histological Injury but Not Tissue Inflammation in a Sheep Model of Pregnancy.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- Biophysically stressed vascular smooth muscle cells express MCP-1The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2024Article
- Amnion responses to intrauterine inflammation and effects of inhibition of TNF signaling in preterm Rhesus macaque.iScience · 2023Article
- The role of neutrophils in chorioamnionitis.Frontiers in immunology · 2023Review
- Possible important roles of galectins in the healing of human fetal membranes.Frontiers in endocrinology · 2022Review
- Betamethasone as a potential treatment for preterm birth associated with sterile intra-amniotic inflammation: a murine study.Journal of perinatal medicine · 2021Article
- Article
- 5-LO-derived LTB4 plays a key role in MCP-1 expression in HMGB1-exposed VSMCs via a BLTR1 signaling axis.Scientific reports · 2021Article
- Understanding Host-Pathogen Interactions in Acute Chorioamnionitis Through the Use of Animal Models.Frontiers in cellular and infection microbiology · 2021Review
- High-mobility group box 1 is a driver of inflammation throughout pregnancy.American journal of reproductive immunology (New York, N.Y. : 1989) · 2021Review
- The Role of Danger Associated Molecular Patterns in Human Fetal Membrane Weakening.Frontiers in physiology · 2020Review
- Immunobiology of Acute Chorioamnionitis.Frontiers in immunology · 2020Review
- High mobility group box protein 1 neutralization therapy in ovine bacteremia: Lessons learned from an ovine septic shock model incorporating intensive care support.Experimental and therapeutic medicine · 2019Article
- IL-1 signaling mediates intrauterine inflammation and chorio-decidua neutrophil recruitment and activation.JCI insight · 2018Article
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Authors and funding
7 authors at 4 institutions in 3 countries.
Funding
Abstract
unlabelledTo understand the changes in the structural integrity of fetal membranes during intrauterine inflammation, we evaluated the time course of expression and localization of damage-associated molecular patterns (DAMPs) and injury/remodeling in collagen and vascular smooth muscle. Time-mated ewes received intra-amniotic (IA) saline or IA lipopolysaccharide (LPS) for 5 hours to 15 days prior to a preterm delivery at 125 ± 2 days (n = 5-7 animals/group). The DAMP high mobility group box 1 (HMGB1) protein assessed by Western blot was induced within 24 hours after IA LPS in the fetal membranes, and HMGB1 expression was localized to amnion epithelium, chorion vascular endothelium, and infiltrating inflammatory cells by immunohistology. Markers of vascular injury, intercellular adhesion molecule 1, and tissue plasminogen activator messenger RNA (mRNA) expression increased 5 to 12 hours after IA LPS in the chorioamnion indicating vascular injury. Chorion vascular remodeling with increased chorion arteriolar smooth muscle actin expression by morphometric analyses of immunohistology was noted 15 days after IA LPS. Collagen expression was nonhomogeneous by histochemical staining, and there was a trend toward decreased mRNA expression of collagen subunit COL5A1 after IA LPS.
conclusionsIntrauterine inflammation induced early increases in HMGB1 in the chorioamnion with a concomitant vascular injury followed by chorion arteriolar hypertrophy. There was nonhomogeneous collagen expression in the chorioamnion. These results have implications for understanding the pathogenesis of IA inflammation-induced preterm rupture of membranes.
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