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长链非编码 RNA TNK2-AS1 通过海绵吸附 miR-150-5p 调节 VEGFA 和 FGF1 的表达来调控 ox-LDL 刺激的 HASMC 增殖和迁移。

LncRNA TNK2-AS1 regulated ox-LDL-stimulated HASMC proliferation and migration via modulating VEGFA and FGF1 expression by sponging miR-150-5p.

机构信息

Department of Cardiology, the First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.

Department of Cardiology, the First Affiliated Hospital of Xi'an Medical University, Xi'an, China.

出版信息

J Cell Mol Med. 2019 Nov;23(11):7289-7298. doi: 10.1111/jcmm.14575. Epub 2019 Aug 29.

DOI:10.1111/jcmm.14575
PMID:31468685
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6815783/
Abstract

Long non-coding RNAs (lncRNAs) have been indicated for the regulatory roles in cardiovascular diseases. This study determined the expression of lncRNA TNK2 antisense RNA 1 (TNK2-AS1) in oxidized low-density lipoprotein (ox-LDL)-stimulated human aortic smooth muscle cells (HASMCs) and examined the mechanistic role of TNK2-AS1 in the proliferation and migration of HASMCs. Our results demonstrated that ox-LDL promoted HASMC proliferation and migration, and the enhanced proliferation and migration in ox-LDL-treated HASMCs were accompanied by the up-regulation of TNK2-AS1. In vitro functional studies showed that TNK2-AS1 knockdown suppressed cell proliferation and migration of ox-LDL-stimulated HASMCs, while TNK2-AS1 overexpression enhanced HASMC proliferation and migration. Additionally, TNK2-AS1 inversely regulated miR-150-5p expression via acting as a competing endogenous RNA (ceRNA), and the enhanced effects of TNK2-AS1 overexpression on HASMC proliferation and migration were attenuated by miR-150-5p overexpression. Moreover, miR-150-5p could target the 3' untranslated regions of vascular endothelial growth factor A (VEGFA) and fibroblast growth factor 1 (FGF1) to regulate FGF1 and VEGFA expression in HASMCs, and the inhibitory effects of miR-150-5p overexpression in ox-LDL-stimulated HASMCs were attenuated by enforced expression of VEGFA and FGF1. Enforced expression of VEGFA and FGF1 also partially restored the suppressed cell proliferation and migration induced by TNK2-AS1 knockdown in ox-LDL-stimulated HASMCs, while the enhanced effects of TNK2-AS1 overexpression on HASMC proliferation and migration were attenuated by the knockdown of VEGFA and FGF1. Collectively, our findings showed that TNK2-AS1 exerted its action in ox-LDL-stimulated HASMCs via regulating VEGFA and FGF1 expression by acting as a ceRNA for miR-150-5p.

摘要

长链非编码 RNA（lncRNA）在心血管疾病的调控中具有重要作用。本研究旨在探讨 lncRNA TNK2 反义 RNA 1（TNK2-AS1）在氧化型低密度脂蛋白（ox-LDL）刺激的人主动脉平滑肌细胞（HASMCs）中的表达，并研究 TNK2-AS1 在 HASMCs 增殖和迁移中的作用机制。结果表明，ox-LDL 促进 HASMC 的增殖和迁移，ox-LDL 处理的 HASMC 中 TNK2-AS1 的上调伴随着增殖和迁移的增强。体外功能研究表明，TNK2-AS1 敲低抑制 ox-LDL 刺激的 HASMC 增殖和迁移，而过表达 TNK2-AS1 则增强 HASMC 的增殖和迁移。此外，TNK2-AS1 通过作为竞争性内源性 RNA（ceRNA）反式调控 miR-150-5p 的表达，而 miR-150-5p 过表达减弱了 TNK2-AS1 过表达对 HASMC 增殖和迁移的增强作用。此外，miR-150-5p 可以靶向血管内皮生长因子 A（VEGFA）和成纤维细胞生长因子 1（FGF1）的 3'UTR 来调节 HASMC 中 FGF1 和 VEGFA 的表达，而 miR-150-5p 过表达对 ox-LDL 刺激的 HASMCs 的抑制作用被 VEGFA 和 FGF1 的强制表达所减弱。VEGFA 和 FGF1 的强制表达也部分恢复了 TNK2-AS1 敲低对 ox-LDL 刺激的 HASMCs 中增殖和迁移的抑制作用，而过表达 TNK2-AS1 对 HASMC 增殖和迁移的增强作用则被 VEGFA 和 FGF1 的敲低所减弱。综上所述，我们的研究结果表明，TNK2-AS1 通过作为 miR-150-5p 的 ceRNA 调节 VEGFA 和 FGF1 的表达，从而在 ox-LDL 刺激的 HASMCs 中发挥作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a7a/6815783/57e7d77368b6/JCMM-23-7289-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a7a/6815783/ce3ddc1c5380/JCMM-23-7289-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a7a/6815783/bdbe6ef637a6/JCMM-23-7289-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a7a/6815783/c68b15ec8cc0/JCMM-23-7289-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a7a/6815783/e9463df8407e/JCMM-23-7289-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a7a/6815783/40aed829640e/JCMM-23-7289-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a7a/6815783/57e7d77368b6/JCMM-23-7289-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a7a/6815783/ce3ddc1c5380/JCMM-23-7289-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a7a/6815783/bdbe6ef637a6/JCMM-23-7289-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a7a/6815783/c68b15ec8cc0/JCMM-23-7289-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a7a/6815783/e9463df8407e/JCMM-23-7289-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a7a/6815783/40aed829640e/JCMM-23-7289-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a7a/6815783/57e7d77368b6/JCMM-23-7289-g006.jpg

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