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宫内母体免疫激活后对小鼠皮质发生的连续扰动。

Sequential perturbations to mouse corticogenesis following in utero maternal immune activation.

机构信息

Center for Neuroscience, UC Davis, Davis, United States.

Department of Pediatrics & Human Development, Michigan State University, East Lansing, United States.

出版信息

Elife. 2021 Mar 5;10:e60100. doi: 10.7554/eLife.60100.

DOI:10.7554/eLife.60100
PMID:33666173
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7979158/
Abstract

In utero exposure to maternal immune activation (MIA) is an environmental risk factor for neurodevelopmental and neuropsychiatric disorders. Animal models provide an opportunity to identify mechanisms driving neuropathology associated with MIA. We performed time-course transcriptional profiling of mouse cortical development following induced MIA via poly(I:C) injection at E12.5. MIA-driven transcriptional changes were validated via protein analysis, and parallel perturbations to cortical neuroanatomy were identified via imaging. MIA-induced acute upregulation of genes associated with hypoxia, immune signaling, and angiogenesis, by 6 hr following exposure. This acute response was followed by changes in proliferation, neuronal and glial specification, and cortical lamination that emerged at E14.5 and peaked at E17.5. Decreased numbers of proliferative cells in germinal zones and alterations in neuronal and glial populations were identified in the MIA-exposed cortex. Overall, paired transcriptomic and neuroanatomical characterization revealed a sequence of perturbations to corticogenesis driven by mid-gestational MIA.

摘要

子宫内暴露于母体免疫激活（MIA）是神经发育和神经精神疾病的环境风险因素。动物模型为确定与 MIA 相关的神经病理学驱动机制提供了机会。我们通过在 E12.5 时注射 poly(I:C) 对诱导的 MIA 进行了小鼠皮质发育的时间过程转录谱分析。通过蛋白质分析验证了 MIA 驱动的转录变化，并通过成像鉴定了皮质神经解剖结构的平行干扰。暴露后 6 小时，与缺氧、免疫信号和血管生成相关的基因出现急性上调。紧随其后的是增殖、神经元和神经胶质特化以及皮质分层的变化，这些变化出现在 E14.5 并在 E17.5 达到高峰。在 MIA 暴露的皮质中，生发区的增殖细胞数量减少，神经元和神经胶质群体发生改变。总的来说，配对的转录组和神经解剖学特征揭示了由中孕期 MIA 驱动的皮质发生的一系列干扰。

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