Beyond white matter damage: fetal neuronal injury in a mouse model of preterm birth
Beyond white matter damage: fetal neuronal injury in a mouse model of preterm birth
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DOI：
10.1016/j.ajog.2009.06.013
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发表时间：
2009-09-01
影响因子：
9.8
通讯作者：
Elovitz, Michal A.
中科院分区：
文献类型：
--
作者：
Burd, Inna;Chai, Jinghua;Elovitz, Michal A.
目的：本研究的目的是阐明炎症性早产胎儿神经元损伤的可能机制。利用小鼠早产模型，从胎儿脑中制备以下原代培养：(1)对照神经元（CNs），(2)脂多糖暴露神经元（LNs），(3)由神经元和胶质细胞组成的对照共培养（CCC），(4)由脂多糖暴露神经元和胶质细胞组成的脂多糖暴露共培养（LCC）， cnn， LN， CCC，免疫细胞化学进行培养鉴定和神经元形态学证据，定量检测神经元分化标志物微管相关蛋白2。结果：体内脂多糖暴露不影响共培养中神经元或胶质细胞的含量，但降低了lcc中微管相关蛋白2的表达，而lcc和lcc诱导的对照神经元的形态变化与lcc相似，体内暴露（lcc）引起的神经元损伤不能被对照组的培养基逆转。脂多糖诱导的早产可能导致不可逆的神经元损伤
OBJECTIVE: The purpose of this study was to elucidate possible mechanisms of fetal neuronal injury in inflammation-induced preterm birthSTUDY 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 9RESULTS: 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 groupsCONCLUSION: Lipopolysaccharide-induced preterm birth may be responsible for irreversible neuronal injury