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在肺移植后,LncRNA H19通过KLF5-介导的CCL28激活加剧了初级移植功能障碍

Jiwei Li¹, Zhijun Han¹, Zibo Zhu¹

¹Department of Thoracic Surgery, Zhengzhou Key Laboratory for Surgical Treatment for End-stage Lung Disease, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, People's Hospital of Henan University, Zhengzhou, China.

American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons

|July 2, 2023

概括

在肺移植 (LT) 后,H19通过增加KLF5和CCL28表达来促进初级移植功能障碍 (PGD),导致炎症和细胞损伤. 沉默H19可以减轻PGD.

科学领域:

免疫学免疫学免疫学
分子生物学分子生物学
移植科学移植科学

背景情况:

主要移植功能障碍 (PGD) 是肺移植 (LT) 后的一个主要并发症.
在PGD背后的分子机制,特别是长非编码RNA的作用,仍然不完全理解.

研究的目的:

研究LT后的PGD中长非编码RNAH19的参与.
阐明H19影响PGD的分子机制,重点关注其与KLF5和CCL28.2的相互作用.

主要方法:

高通量转录组测序以识别差异表达的长非编码RNA和信使RNA.
同表达分析以确定潜在的监管网络.
在实验室研究中,使用低氧诱导的人类肺微血管内皮细胞损伤模型与H19敲击.
在体内验证,使用正管左肺移植 (LT) 模型进行验证.

主要成果:

确定H19/KLF5/CCL28信号轴是PGD的一个关键参与者.
在PGD模型中,沉默H19减少了炎症反应,改善了肺功能.
发现H19通过与转录因子KLF5.5相互作用来增强CCL28表达.
内皮细胞的CCL28分泌招募了中性粒细胞和巨细胞,加剧了PGD.

结论:

H19通过对KLF5和随后的CCL28表达进行上调来促进LT之后的PGD.
准H19/KLF5/CCL28通路可能为预防或治疗PGD提供一种新的治疗策略.

关键词:

CCL28 CCL28 CCL28 CCL28 CCL28 CCL28 CCL28 CCL28 H19 H19 是一种H19病毒.在KLF5KLF5KLF5KLF5 高通量转录基因组测序巨细胞是什么?巨细胞是什么?中性粒细胞中性粒细胞.主要的移植功能障碍.

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