Beyond white matter damage: fetal neuronal injury in a mouse model of preterm birth

Irina Burd, Jinghua Chai, Juan Gonzalez, Ella Ofori, Hubert Monnerie, Peter D. Le Roux, Michal A. Elovitz

Research output: Contribution to journalArticlepeer-review

45 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)279.e1-279.e8
JournalAmerican journal of obstetrics and gynecology
Issue number3
StatePublished - Sep 2009
Externally publishedYes


  • mouse model
  • neuroinflammation
  • neuronal injury
  • preterm birth

ASJC Scopus subject areas

  • Obstetrics and Gynecology


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