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希斯甲基化调节中性粒细胞外细胞陷,以减弱角膜新血管化的作用

Yujie Mou¹, Shuo Yang¹, Jiayun Yu¹

¹Eye Center, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310009, PR China; Zhejiang Provincial Key Lab of Ophthalmology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310009, PR China.

International immunopharmacology

|November 5, 2024

概括

中性粒细胞外细胞陷 (NETs) 有助于角膜新血管化 (CNV). 歇斯甲基化调节NETs,并通过JIB-04抑制它通过向NF-κB/ERK/ROS通路来减少CNV.

科学领域:

眼科医生眼科眼科
免疫学免疫学免疫学
分子生物学分子生物学

背景情况:

角膜新血管化 (CNV) 会损害视力和眼睛的健康.
驱动CNV的机制,特别是中性粒细胞外细胞陷 (NETs) 的作用,尚未完全理解.
在CNV的背景下,素甲基化对NET的影响需要进行研究.

研究的目的:

研究中性粒细胞外细胞陷 (NETs) 在角膜新血管化 (CNV) 中的作用.
探索 histone 甲基化如何调节 CNV 期间 NETs 的形成.
评估向质子甲基化的治疗潜力,以治疗NV.

主要方法:

使用烧来诱导一个CNV小鼠模型.
隔离和刺激人类初级中性粒细胞形成NET.
转录组分析以确定NETs参与角膜烧.
用基脱甲基酶抑制剂JIB-04调节NETs基甲基化.
血管新生和炎症的体外和体内评估.

主要成果:

NETs在烧引起的CNV中起着显著的作用,并且可以被NaOH刺激.
孤立的NETs加剧了CNV,促进了血管内皮细胞迁移,增殖和管道形成.
在体内和体内血管新生和炎症中改善了NETs的破坏.
性燃烧抑制了NETs基因组甲基化,该基因组甲基化被JIB-04.4恢复.
通过调节NF-κB/ERK/ROS通路,JIB-04治疗减少了CNV和NETs的形成.

结论:

歇斯甲基化在调节NETs形成和随后的血管生成中发挥着关键作用.
向组织蛋白甲基化,例如JIB-04,为CNV提供了一个新的治疗策略.
这项研究发现了一种新的机制,它将组织素甲基化,NET和血管生成联系在一起,为新血管化相关疾病提供了潜在的治疗方法.

关键词:

角膜新血管化的情况.希斯甲基化希斯甲基化 NF-kappa B信号通道的信号通道中性粒细胞外细胞陷反应性氧物种的反应性氧物种.

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