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首页> 外文期刊>Folia neuropathologica >Disturbed maturation of oligodendrocyte progenitors in lipopolysaccharide-induced hypomyelination in cultured forebrain slices of neonatal rats
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Disturbed maturation of oligodendrocyte progenitors in lipopolysaccharide-induced hypomyelination in cultured forebrain slices of neonatal rats

机译：脂多糖诱导的新生大鼠培养前脑切片中少突胶质细胞祖细胞的成熟紊乱

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Introduction This study was performed to determine whether the disturbed maturation of oligodendrocyte (OL) progenitors might be related to lipopolysaccharide (LPS)-induced hypomyelination. Material and methods We created organotypic cultures of forebrain slices from neonatal rats and explored the morphological changes of glial cells expressing tumour necrosis factor ? (TNF-?) following LPS exposure. Results We observed marked activation of glial fibrillary acidic protein-positive astrocytes and OX42-positive microglia co-labelled with TNF-? four days following LPS exposure. Our results further demonstrated a?reduced expression of O4-positive and O1-positive OL progenitors; moreover, we found that their morphologies were suggestive of degeneration (e.g., scanty, rounded bodies with short, fragmented processes and/or cytoplasmic condensation). At seven days following LPS exposure, astrocytes and microglia were still co-labelled for TNF-?; however, the expression of O4-positive and O1-positive cells somewhat increased compared to the number observed at 4 days; despite remaining undifferentiated and exhibiting immature morphologies, the cells were likely indicative of regeneration. In contrast, O4-positive and O1-positive cells in controls were well-differentiated, displaying round, thick cell bodies and long, branching processes. Conclusions In conclusion, maturation arrest and/or under-differentiation of OL progenitors commonly occur during regeneration: they may underlie the degeneration and consequent hypomyelination occurring late after injury, or apoptosis during the acute stage post-injury. Microglia and astrocytes expressing TNF-? may also contribute to later myelination failure.
机译：引言进行这项研究是为了确定少突胶质细胞（OL）祖细胞成熟是否与脂多糖（LPS）诱导的髓鞘过少有关。材料和方法我们创建了新生大鼠前脑切片的器官型培养物，并探讨了表达肿瘤坏死因子α的神经胶质细胞的形态变化。 LPS暴露后（TNF-α）。结果我们观察到与TNF-α共标记的神经胶质纤维酸性蛋白阳性星形胶质细胞和OX42阳性小胶质细胞明显活化。 LPS暴露后四天。我们的结果进一步证明了O4阳性和O1阳性OL祖细胞的表达降低。此外，我们发现它们的形态暗示了变性（例如，矮小的，圆形的体，具有短的，破碎的过程和/或细胞质凝缩）。 LPS暴露后第7天，星形胶质细胞和小胶质细胞仍被TNF-α标记。然而，与4天时观察到的数目相比，O4阳性和O1阳性细胞的表达有所增加。尽管仍保持未分化状态并表现出未成熟的形态，但细胞仍可能指示再生。相比之下，对照组中的O4阳性和O1阳性细胞分化良好，显示出圆形，厚实的细胞体和较长的分支过程。结论总之，OL祖细胞的成熟停滞和/或分化不足通常发生在再生过程中：它们可能是损伤后变性，继发性髓鞘过少或受伤后急性阶段凋亡的基础。表达TNF-α的小胶质细胞和星形胶质细胞也可能导致以后的髓鞘衰竭。

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