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介酶干细胞衍生的外体miR-27b-3p通过降低YAP/LOXL2通路的调节减轻肝纤维化

Fang Cheng^1,2, Fuji Yang^1,2, Yanjin Wang^1,2

¹Department of Laboratory Medicine, Wujin Hospital Affiliated with Jiangsu University, Jiangsu University, Changzhou, 213017, China.

Journal of nanobiotechnology

|June 16, 2023

概括

人类带衍生的外体细胞 (MSC-ex) 通过抑制类似于lysyl oxidase的2 (LOXL2) 来降低肝纤维化. 外体miR-27b-3p降低了LOXL2的关键调节者YAP的下调,为肝纤维化提供了一个新的治疗策略.

科学领域:

生物化学生化学
细胞生物学细胞生物学
再生医学是一种再生医学.

背景情况:

类似酸氧化酶2 (LOXL2) 在肝纤维化中至关重要,促进原的交叉连接和沉积.
治疗性抑制LOXL2在抑制和逆转肝纤维化方面显示出有前途.
人类带衍生的外体细胞 (MSC-ex) 正在研究其潜在的治疗效果.

研究的目的:

为了研究MSC-ex在抑制肝纤维化中的LOXL2的疗效.
阐明MSC-ex发挥其抗纤维菌作用的潜在分子机制.

主要方法:

碳四化物 (CCl4) 诱导的肝纤维化模型 in vivo.
使用MSC-ex,非选择性LOX抑制剂 (BAPN) 或PBS.
通过组织学和生物化学分析评估血清LOXL2和原交联.
在人肝星状细胞系 (LX-2) 中使用RNA测序和光 in situ杂交 (FISH) 检测MSC-ex机制.

主要成果:

系统性MSC-ex的使用显著降低了LOXL2表达和原交叉连接,延迟了纤维化进展.
富含MSC-ex的miR-27b-3p被发现通过准其在LX-2细胞中的3' UTR来抑制YES相关蛋白 (YAP).
LOXL2被确定为YAP的下游目标,YAP积极调节LOXL2转录.
抑制miR-27b-3p取消了MSC-ex的抗LOXL2活性和抗纤维素作用,而过度表达增强了它们.

结论:

通过外体miR-27b-3p调节YAP的下调,MSC-ex抑制LOXL2表达和肝纤维化进展.
这一途径突显出一种新的机制,用于肝纤维化中的基于外体的治疗.
这些发现为使用MSC-ex.的肝纤维化治疗提供了新的治疗途径.

关键词:

原的交叉连接.异构体是什么? 异构体是什么? 外构体是什么?在LOXL2中使用LOXL2.肝脏纤维化肝脏纤维化在MSC中,MSC是MSC.哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈在 miR-27b-3p 中.

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