由BMSC衍生的外体miR-148b-3p通过准DLL4和Notch1来减弱OGD/R诱导的HMC3细胞激活
Fang Yi1, Hui Xiao2, Mingyu Song3
1Department of Geriatric Neurology, Xiangya Hospital, Central South University, Changsha 410008, Hunan, PR China; National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, Hunan 410008, PR China.
携带miR-148b-3p的骨髓干细胞衍生外体 (BMSC-Exo) 可以通过DLL4/Notch1通路抑制微质激活来治疗缺血性损伤.
科学领域:
- 生物医学科学 生物医学科学
- 细胞生物学 细胞生物学
- 神经科学是一个神经科学.
背景情况:
- 缺血性脑血管疾病 (IC) 涉及微质激活,导致神经元损伤.
- 骨髓介质干细胞 (BMSC) 衍生的外体细胞 (BMSC-Exo) 对缺血性损伤表现出潜在的治疗作用.
- 了解BMSC-Exo在微质激活中的调节机制对于开发有效的治疗方法至关重要.
研究的目的:
- 研究BMSC-Exo miR-148b-3p在调节氧-葡萄糖剥夺/氧化恢复 (OGD/R) 诱导的微质激活中的作用.
- 阐明涉及Delta类联结体4 (DLL4) 和神经源局部隙同类蛋白1 (Notch1) 的潜在分子机制.
主要方法:
- 使用传输电子显微镜 (TEM) 和qNano.使用BMSC-Exo的表征.
- 通过MTT,流细胞测量,划痕,穿孔和ELISA测试来评估HMC3细胞激活.
- 双露西法酶记者测定证实了miR-148b-3p和DLL4/Notch1.1之间的向关系.
主要成果:
- OGD/R降低了HMC3细胞中的miR-148b-3p表达;BMSC-Exo治疗上调了miR-148b-3p.
- BMSC-Exo抑制了OGD/R诱导的HMC3细胞活力,迁移和促炎性细胞因子释放,同时促进了G0/G1阶段的停止.
- miR-148b-3p直接针对DLL4和Notch1,并且其对DLL4/Notch1减弱的OGD/R诱导的微质激活的抑制或抑制.
结论:
- 通过准DLL4和Notch1.1,BMSC-Exo miR-148b-3p有效地抑制了OGD/R诱导的微质激活.
- 这一途径为治疗脑缺血症提供了一种新的治疗策略.
- 作为治疗缺血性脑血管疾病的方法,BMSC-Exo miR-148b-3p具有显著的前景.
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