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通过circ_0001103将巨细胞向肌纤维细胞过渡为目标,用于治疗亚细纤维化

Qi Zhang^1,2, Bing Lu³, Lei He⁴

¹Department of Ophthalmology, The First Affiliated Hospital of Wannan Medical College (Yijishan Hospital of Wannan Medical College), Wuhu, 241001, Anhui, People's Republic of China.

Journal of translational medicine

|February 28, 2025

概括

循环RNAcirc_0001103通过调节巨细胞到肌纤维细胞过渡 (MMT) 来促进亚皮纤维化. 抑制circ_0001103在与年龄相关的黄斑变性模型中抑制纤维化和泄漏.

科学领域:

眼科医生眼科眼科
分子生物学分子生物学
细胞生物学细胞生物学

背景情况:

亚视网膜纤维化是与年龄相关的黄斑变性 (AMD) 视力丧失的关键原因.
驱动子纤维化的精确机制仍然不完全理解.
巨细胞到肌纤维细胞的过渡 (MMT) 与纤维化过程有关.

研究的目的:

调查MMT在脑下纤维化发展中的作用.
为了确定circ_0001103是否通过MMT调节下纤维化形成.

主要方法:

建立了一种激光诱导的脑下腺纤维化和胆道新血管化 (CNV) 的小鼠模型.
利用微阵列分析来识别改变的circRNAs.
采用免疫组织化学,双化酶记者测定,FISH,RNA免疫沉,qRT-PCR和西部斑点来分析分子相互作用和MMT.
通过静脉内注射与circ_0001103进行干预,以评估功能影响.

主要成果:

在CNV小鼠模型中确定了58个显著改变的circRNA.
观察到MMT和子皮膜纤维化中circ_0001103的表达增加.
证明了circ_0001103的海绵miR-7240-5p,针对SLC9A调节MMT.
表明抑制circ_0001103可以抑制MMT,膜纤维化和CNV泄漏.

结论:

通过调节SLC9A1介导的MMT,circ_0001103促进子皮膜纤维化和中枢神经漏.
抑制circ_0001103为AMD相关的视力损失提供了潜在的治疗策略.

关键词:

与年龄相关的黄斑变性.巨细胞转变为肌纤维细胞.亚视网膜纤维化是什么 circ_0001103 在线阅读在 miR-7240-5p 中使用.

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