在Notch3淘汰赛和糖尿病小鼠中,细胞与血管内皮细胞形成了膨胀的连接
Timothy E Vanderleest1, Harper B Gordon1, Michael O'Hare1
1Schepens Eye Research Institute of Mass Eye and Ear and the Department of Ophthalmology at Harvard Medical School, Boston, Massachusetts 02114, USA.
在缺乏Notch3信号或患有糖尿病的小鼠中,细胞-内皮细胞连接显示出大. 这表明细胞增加接触,以补偿被破坏的Notch3信号,影响微血管健康.
科学领域:
- 血管生物学 血管生物学
- 细胞超结构 细胞超结构
- 糖尿病并发症 糖尿病并发症
背景情况:
- 细胞对于微血管健康至关重要,直接与内皮细胞相互作用.
- 周细胞-内皮细胞接触的功能意义,特别是超结构性变化,尚不清楚.
- 诺奇3信号涉及血管细胞通信,其破坏与糖尿病视网膜病变有关.
研究的目的:
- 为了研究皮细胞-内皮细胞相互作用中的超结构性形态变化.
- 为了检查缺乏Notch3受体的小鼠和糖尿病视网膜病变模型中的这些变化.
- 了解这些细胞接触在疾病状态中的功能意义.
主要方法:
- 连续截面传输电子显微镜 (ssTEM) 用于对小鼠视网膜中的毛细血管进行成像.
- 分析包括野生类型,Notch3淘汰赛,有条件的Notch3淘汰赛和糖尿病小鼠模型.
- 自动图像分析量化了皮细胞和内皮细胞之间的接触长度和和插孔特征.
主要成果:
- 诺奇3淘汰器体表现出更深的钉子和增加的围细胞-内皮细胞连接性.
- 无论是诺奇3淘汰赛还是糖尿病病症,都显示出细胞周围的尺寸增加.
- 在分析的组中,容器直径和细胞覆盖面仍然相似.
结论:
- 在Notch3淘汰赛和糖尿病病症中,扩大的细胞周钉表明存在补偿机制.
- 接触面积的增加可能是由于Notch3信号的丧失造成的.
- 这些发现强调了Notch3信号在调节细胞内皮细胞相互作用和微血管完整性方面的作用.
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