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Assessment of Kidney Function in Mouse Models of Glomerular Disease
Published on: June 30, 2018
通过失调的血管生成和炎症反应加剧了SerpinE2缺乏糖尿病脏损伤
Leila Idir1, Junjie Yu1, Philippe Bonnin1,2
1LVTS, INSERM U1148, Université Paris Cité and Université Sorbonne Paris Nord, F-75018 Paris.
在小鼠中,SerpinE2 缺乏会使糖尿病病变 (DN) 恶化,增加淋巴细胞损伤,炎症和功能受损. 这表明SerpinE2在DN进展中起着保护作用.
科学领域:
- 肝脏病学
- 内分泌学
- 分子生物学
背景情况:
- 糖尿病病 (DN) 涉及复杂的炎症和血管生成.
- 塞尔E2 (蛋白酶内-1) 是血管和炎症细胞表达的蛋白酶抑制剂.
研究的目的:
- 研究SerpinE2在糖尿病病的发展中的作用.
- 阐明SerpinE2在糖尿病中影响损伤的机制.
主要方法:
- 使用链杆菌素诱导的1型和db/db2型糖尿病小鼠模型.
- 将SerpinE2淘汰赛 (SerpinE2-/-) 的小鼠与野生型 (WT) 的 littermates进行比较.
- 评估了组织学特征,功能 (尿中的白蛋白与肌素的比例),球血管化,细胞增殖和炎症性细胞因子mRNA水平.
主要成果:
- 糖尿病小鼠表现出恶化的脏病,包括质缩,IV原蛋白增加和氨酸表达减少.
- 在SerpinE2-小鼠中,功能受损,白尿率较高.
- 在糖尿病患者的SerpinE2-脏中观察到球血管化,细胞增殖和炎症性细胞因子mRNA水平的增加.
结论:
- 在糖尿病病中,SerpinE2似乎起着保护作用.
- 通过调节血管新生和炎症的早期过程,SerpinE2 限制了球膜损伤.
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