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长链非编码RNA uc003pxg.1与miR-339-5p相互作用促进血管内皮细胞增殖、迁移和血管生成。

LncRNA uc003pxg.1 Interacts With miR-339-5p Promote Vascular Endothelial Cell Proliferation, Migration and Angiogenesis.

作者信息

Li Ping, Wang Feng, Yue Anna, Xuan Yanling, Huang Ying, Xu Jingyi, Weng Jiayi, Li Yuan, Sun Kangyun

机构信息

Department of Cardiology, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Gusu School, Nanjing Medical University, Suzhou, P. R. China.

Department of Central Laboratory, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Gusu School, Nanjing Medical University, Suzhou, P. R. China.

出版信息

Korean Circ J. 2025 May;55(5):440-455. doi: 10.4070/kcj.2024.0153. Epub 2024 Nov 18.

DOI:10.4070/kcj.2024.0153
PMID:39733458
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12088996/
Abstract

BACKGROUND AND OBJECTIVES

This study aimed to investigate the roles of lncRNA uc003pxg.1 and miR-339-5p in regulating the occurrence and development of coronary heart disease.

METHODS

First, the expression levels of uc003pxg.1 and miR-339-5p were verified in peripheral blood mononuclear cells of clinical samples. Then, the target gene was identified using high-throughput sequencing combined with bioinformatics. Human umbilical vein endothelial cells (HUVECs) were transfected with si-uc003pxg.1, miR-339-5p mimic and miR-339-5p inhibitor, and the expression of related genes was detected by reverse transcription-quantitative polymerase chain reaction and western blotting. EdU, CCK-8, Cell scratch and Transwell assays were used to analyze the effects of uc003pxg.1 and miR-339-5p on cell proliferation and migration.

RESULTS

The expression of uc003pxg.1 and miR-339-5p was negatively correlated in clinical samples and HUVECs. The si-uc003pxg.1 and miR-339-5p mimic decreased the proliferation and migration of HUVECs and decreased the expression of transforming growth factor (TGF)-β1 and α-smooth muscle actin (SMA). The protein expression levels of TGF-β1, α-SMA, CD31, collagen I, collagen III and endoglin were decreased, and angiogenesis was weakened. The miR-339-5p inhibitor had the opposite effect.

CONCLUSIONS

Our study revealed that upregulation of uc003pxg.1 and downregulation of miR-339-5p in vitro promote cell proliferation, cell migration and angiogenesis and upregulate the expression of TGF-β1, α-SMA, CD31, collagen I, collagen III and endoglin, which may lead to the development of vascular atherosclerosis.

摘要

背景与目的

本研究旨在探讨长链非编码RNA uc003pxg.1和miR-339-5p在冠心病发生发展过程中的调控作用。

方法

首先，在临床样本的外周血单个核细胞中验证uc003pxg.1和miR-339-5p的表达水平。然后，采用高通量测序结合生物信息学方法鉴定靶基因。将小干扰RNA-uc003pxg.1、miR-339-5p模拟物和miR-339-5p抑制剂转染人脐静脉内皮细胞（HUVECs），通过逆转录-定量聚合酶链反应和蛋白质印迹法检测相关基因的表达。采用EdU、CCK-8、细胞划痕和Transwell实验分析uc003pxg.1和miR-339-5p对细胞增殖和迁移的影响。

结果

在临床样本和HUVECs中，uc003pxg.1和miR-339-5p的表达呈负相关。小干扰RNA-uc003pxg.1和miR-339-5p模拟物降低了HUVECs的增殖和迁移能力，并降低了转化生长因子（TGF）-β1和α-平滑肌肌动蛋白（SMA）的表达。TGF-β1、α-SMA、CD31、I型胶原、III型胶原和内皮糖蛋白的蛋白表达水平降低，血管生成减弱。miR-339-5p抑制剂则产生相反的效果。

结论

我们的研究表明，体外上调uc003pxg.1和下调miR-339-5p可促进细胞增殖、细胞迁移和血管生成，并上调TGF-β1、α-SMA、CD31、I型胶原、III型胶原和内皮糖蛋白的表达，这可能导致血管动脉粥样硬化的发展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28b8/12088996/861cc8652d34/kcj-55-440-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28b8/12088996/04e5f6861fbe/kcj-55-440-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28b8/12088996/0f944d631584/kcj-55-440-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28b8/12088996/814efa72bd27/kcj-55-440-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28b8/12088996/23cbe570a014/kcj-55-440-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28b8/12088996/861cc8652d34/kcj-55-440-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28b8/12088996/04e5f6861fbe/kcj-55-440-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28b8/12088996/0f944d631584/kcj-55-440-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28b8/12088996/814efa72bd27/kcj-55-440-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28b8/12088996/23cbe570a014/kcj-55-440-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28b8/12088996/861cc8652d34/kcj-55-440-g005.jpg

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