外体通过心脑与大脑的长距离通信来激活大脑动中海马的微质
Xuewen Wang1,2,3,4, Yuanjia Ke1,2,3, Zhen Cao1,2,3
1Department of Cardiology, Renmin Hospital of Wuhan University, 238 Jiefang Road, Wuhan, 430060, Hubei, China.
BMC cardiovascular disorders
|November 8, 2024
概括
心房动 (AF) 可以通过激活大脑微质来导致认知障碍 (CI). AF衍生的外体携带cfa-miR-22e,该外体在海马中准IL33,导致CI.
科学领域:
- 神经科学是一个神经科学.
- 心脏病学 心脏病学
- 分子生物学分子生物学
背景情况:
- 心房动 (AF) 越来越被认为是认知障碍 (CI) 和痴呆症的危险因素.
- 独立于中风,将AF与CI联系在一起的精确机制需要进一步阐明.
研究的目的:
- 研究由心房动 (AF) 引起的认知障碍 (CI) 的潜在机制.
- 探索从上心脂肪组织 (EAT) 衍生出来的外体在AF相关CI中的作用.
主要方法:
- 在使用快速心房节奏的狗中建立了AF模型,并用GW4869治疗以抑制外体细胞功能.
- 使用Ad-CD63-RFP追踪EAT衍生的外体,并通过测序和qRT-PCR分析它们的RNA含量.
- 通过生物信息学和光酶测定研究了外体向相互作用,并在体内和体外评估了微质激活.
主要成果:
- 引发AF导致AF持续时间增加,并提高了EAT和海马体内的外体cfa-miR-22e水平.
- 在AF犬的海马中观察到目标基因IL33的下调.
- 治疗GW4869减轻了这些分子变化,而体外研究证实了这些发现.
结论:
- 在AF犬中,心膜脂肪组织 (EAT) 释放出穿越血脑屏障 (BBB) 的外体.
- 这些外体通过cfa-miR-22e/IL33信号通路激活海马微质,导致认知障碍 (CI).
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