Scholarlink

<p>Maternal preeclampsia (PE) contributes to neurodevelopmental disorders. However, the underlying molecular mechanism remains unclear. We investigated the potential biological regulatory mechanisms by establishing an animal model and primary cell culture. Data from the Adolescent Brain Cognitive Development human study revealed that the striatum mediates maternal PE and offspring behavioral disorders. In a rat PE model, offspring exhibited abnormal behaviors and reduced striatal vascular density, with disrupted blood-brain barrier (BBB) and swollen astrocytes. Primary astrocytes and brain microvascular endothelial cells (BMECs) were cultured. Astrocytes from PE-exposed offspring weakened tube-formation ability and BBB-related protein expression in BMECs. Transcript sequencing identified B-cell lymphoma 2 (BCL2) as a key neurodevelopmental gene affected by PE. Astrocytes with BCL2 knockdown weakened tube-formation and BBB-related protein expression in BMECs, matching PE offspring astrocytes. BCL2 knockdown in newborn rats resulted in disrupted BBB, and abnormal behaviors, similar to PE-exposed offspring. In summary, reduced astrocyte BCL2 levels contributed to BBB disruption in the striata of PE-exposed offspring, providing new insights into the mechanisms underlying neurodevelopmental disorders.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Reduced BCL2 level in astrocytes contributes to blood-brain barrier disruption in the striatum of offspring exposed to maternal preeclampsia

  • 期刊论文

  • 发表日期：

    2026年6月2日

查看全文
  • Jiashuo Zhang,
  • Mengting Zhang,
  • Zhengyang Zhao,
  • Min Xie,
  • Menghan Wei,
  • Siyi Liu,
  • Yulu Wu,
  • Shiwan Tao,
  • Qiuyue Lv,
  • Xiaoying Ma,
  • Yunqi Huang,
  • Mingli Li,
  • Min Zou,
  • Qiang Wang

摘要

Maternal preeclampsia (PE) contributes to neurodevelopmental disorders. However, the underlying molecular mechanism remains unclear. We investigated the potential biological regulatory mechanisms by establishing an animal model and primary cell culture. Data from the Adolescent Brain Cognitive Development human study revealed that the striatum mediates maternal PE and offspring behavioral disorders. In a rat PE model, offspring exhibited abnormal behaviors and reduced striatal vascular density, with disrupted blood-brain barrier (BBB) and swollen astrocytes. Primary astrocytes and brain microvascular endothelial cells (BMECs) were cultured. Astrocytes from PE-exposed offspring weakened tube-formation ability and BBB-related protein expression in BMECs. Transcript sequencing identified B-cell lymphoma 2 (BCL2) as a key neurodevelopmental gene affected by PE. Astrocytes with BCL2 knockdown weakened tube-formation and BBB-related protein expression in BMECs, matching PE offspring astrocytes. BCL2 knockdown in newborn rats resulted in disrupted BBB, and abnormal behaviors, similar to PE-exposed offspring. In summary, reduced astrocyte BCL2 levels contributed to BBB disruption in the striata of PE-exposed offspring, providing new insights into the mechanisms underlying neurodevelopmental disorders.