自可以通过减少矩阵囊泡体介导的IL-1β释放来减少糖尿病小鼠的大动脉化
Xiaolei Sun1, Yang Zheng2, Linzhuo Xie3
1Department of General Surgery (Vascular Surgery), The Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China; Department of Interventional Medicine, The Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China; Laboratory of Nucleic Acids in Medicine for National High-Level Talents, Nucleic Acid Medicine of Luzhou Key Laboratory, Southwest Medical University, Luzhou, 646000, China; Key Laboratory of Medical Electrophysiology, Ministry of Education & Medical Electrophysiological Key Laboratory of Sichuan Province, Collaborative Innovation Center for Prevention and Treatment of Cardiovascular Disease of Sichuan Province, Institute of Cardiovascular Research, Southwest Medical University, Luzhou, 646000, China; Cardiovascular and Metabolic Diseases Key Laboratory of Sichuan, Luzhou, 646000, China.
携带IL-1β的矩阵囊体 (MVBs) 有助于2型糖尿病的血管化. 自可以抵消这一过程,这表明MVB介导的IL-1β释放是血管化的潜在治疗标.
科学领域:
- 心血管生物学 心血管生物学
- 细胞生物学 细胞生物学
- 糖尿病研究 糖尿病研究
背景情况:
- 血管化 (VC) 是2型糖尿病 (T2DM) 的常见并发症,但其分子机制尚未完全理解.
- 微体和IL-1β与VC病理生理学有关.
研究的目的:
- 研究矩阵囊泡体 (MVB) 和IL-1β在血管化中的作用.
- 探索自在调节这些过程中的潜力.
主要方法:
- 对GEO数据集的分析 GSE146638.8.
- 免疫光 in vivo (糖尿病小鼠模型) 和 in vitro (高葡萄糖VSMC模型).
- 评估MVB数量,IL-1β水平和自标志物.
主要成果:
- 增加了MVB数量,IL-1β水平,以及化大动脉和VSMC中的自.
- IL-1β与MVB和自细胞共局.
- 来自化VSMC的MVB在正常VSMC中诱导化,这种效应通过IL-1β沉默而减少.
- 自调节 (拉帕米辛或氨酸) 影响了IL-1β表达和VSMC化.
结论:
- MVBs调解IL-1β的释放,促进正常VSMC中的VC.
- 自可以对抗MVB介导的IL-1β释放和VC.
- 准MVB介导的IL-1β释放是治疗血管化的有希望的策略.
