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长链非编码 RNA H19 通过靶向 miR-125a-3p/FLT1 轴促进血管新生内膜形成。

lncRNA H19 facilitates vascular neointima formation by targeting miR-125a-3p/FLT1 axis.

机构信息

Department of Cardiology, Ganzhou Hospital of Guangdong Provincial People's Hospital, Ganzhou Municipal Hospital (Gannan Medical University Affiliated Municipal Hospital), Ganzhou 341000, China.

Guangdong Cardiovascular Institute, Guangdong Provincial Key Laboratory of Coronary Heart Disease Prevention, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou 510080, China.

出版信息

Acta Biochim Biophys Sin (Shanghai). 2024 Sep 2;56(10):1437-1445. doi: 10.3724/abbs.2024087.

DOI:10.3724/abbs.2024087
PMID:39238439
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11532204/
Abstract

The aberrant proliferation and migration of vascular smooth muscle cells (VSMCs) contribute to the development of neointima formation in vascular restenosis. This study aims to explore the function of the long noncoding RNA H19 in neointima formation. A mouse carotid ligation model was established, and human vascular smooth muscle cells (VSMCs) were used as a cell model. lncRNA H19 overexpression promoted VSMC proliferation and migration. Moreover, miR-125a-3p potentially bound to lncRNA H19, and Fms-like tyrosine kinase-1 (FLT1) might be a direct target of miR-125a-3p in VSMCs. Upregulation of miR-125a-3p alleviated lncRNA H19-enhanced VSMC proliferation and migration. Furthermore, rescue experiments showed that enhanced expression of miR-125a-3p attenuated lncRNA H19-induced FLT1 expression in VSMCs. In addition, the overexpression of lncRNA H19 significantly exacerbated neointima formation in a mouse carotid ligation model. In summary, lncRNA H19 stimulates VSMC proliferation and migration by acting as a competing endogenous RNA (ceRNA) of miR-125a-3p. lncRNA H19 may be a therapeutic target for restenosis.

摘要

异常增殖和迁移的血管平滑肌细胞(VSMCs)有助于新内膜形成的血管再狭窄。本研究旨在探讨长链非编码 RNA H19 在新内膜形成中的作用。建立了小鼠颈结扎模型，并将人血管平滑肌细胞(VSMCs)作为细胞模型。lncRNA H19 过表达促进 VSMC 增殖和迁移。此外，miR-125a-3p 可能与 lncRNA H19 结合，Fms 样酪氨酸激酶-1 (FLT1)可能是 miR-125a-3p 在 VSMCs 中的直接靶标。上调 miR-125a-3p 减轻了 lncRNA H19 增强的 VSMC 增殖和迁移。此外，挽救实验表明，miR-125a-3p 的过表达减弱了 lncRNA H19 在 VSMCs 中诱导的 FLT1 表达。此外，lncRNA H19 的过表达显著加重了小鼠颈结扎模型中的新内膜形成。总之，lncRNA H19 通过作为 miR-125a-3p 的竞争性内源 RNA (ceRNA) 刺激 VSMC 的增殖和迁移。lncRNA H19 可能是再狭窄的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dba2/11532204/d08e47f2d16d/t7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dba2/11532204/ec40c6cc24fa/t1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dba2/11532204/051db305368d/t3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dba2/11532204/c3c3f2bee1bd/t4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dba2/11532204/fcd5db154a68/t5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dba2/11532204/a3f416c930a4/t6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dba2/11532204/d08e47f2d16d/t7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dba2/11532204/ec40c6cc24fa/t1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dba2/11532204/b14d9341fb81/t2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dba2/11532204/051db305368d/t3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dba2/11532204/c3c3f2bee1bd/t4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dba2/11532204/fcd5db154a68/t5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dba2/11532204/a3f416c930a4/t6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dba2/11532204/d08e47f2d16d/t7.jpg

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