Journal
AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
Volume 201, Issue 3, Pages -Publisher
MOSBY-ELSEVIER
DOI: 10.1016/j.ajog.2009.06.013
Keywords
mouse model; neuroinflammation; neuronal injury; preterm birth
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Funding
- NCRR NIH HHS [UL1RR024134, UL1 RR024134] Funding Source: Medline
- NICHD NIH HHS [R01 HD046544, R01 HD046544-04, 5-R01-HD046544-0] Funding Source: Medline
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OBJECTIVE: The purpose of this study was to elucidate possible mechanisms of fetal neuronal injury in inflammation-induced preterm birth STUDY DESIGN: With 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 RESULTS: Lipopolysaccharide 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 CONCLUSION: Lipopolysaccharide-induced preterm birth may be responsible for irreversible neuronal injury
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