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转录组学为长非编码 RNA HIF1A-AS1 对血管平滑肌细胞调控机制提供新视角。

Transcriptomics Provides Novel Insights into the Regulatory Mechanism of IncRNA HIF1 A-AS1 on Vascular Smooth Muscle Cells.

机构信息

Department of Orthopaedics, The First Affiliated Hospital of Kunming Medical University, Yunnan, People's Republic of China.

出版信息

Braz J Cardiovasc Surg. 2023 Oct 6;38(6):e20220260. doi: 10.21470/1678-9741-2022-0260.

DOI:10.21470/1678-9741-2022-0260
PMID:37801489
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10550220/
Abstract

INTRODUCTION

Thoracic aortic aneurysm is a potentially fatal disease with a strong genetic contribution. The dysfunction of vascular smooth muscle cells (VSMCs) contributes to the formation of this aneurysm. Although previous studies suggested that long non-coding ribonucleic acid (RNA) hypoxia inducible factor 1 α-antisense RNA 1 (HIF1A-AS1) exerted a vital role in the progression and pathogenesis of thoracic aortic aneurysm, we managed to find a new regulatory mechanism of HIF1A-AS1 in VSMCs via transcriptomics.

METHODS

Cell viability was detected by the cell counting kit-8 assay. Cell apoptosis was assessed by Annexin V-fluorescein isothiocyanate/propidium iodide double staining. Transwell migration assay and wound healing assay were performed to check the migration ability of HIF1A-AS1 on VSMCs. The NextSeq XTen system (Illumina) was used to collect RNA sequencing data. Lastly, reverse transcription-quantitative polymerase chain reaction confirmed the veracity and reliability of RNA-sequencing results.

RESULTS

We observed that overexpressing HIF1A-AS1 successfully promoted apoptosis, significantly altered cell cycle distribution, and greatly attenuated migration in VSMCs, further highlighting the robust promoting effects of HIF1A-AS1 to thoracic aortic aneurysm. Moreover, transcriptomics was implemented to uncover its underlying mechanism. A total of 175 differently expressed genes were identified, with some of them enriched in apoptosis, migration, and cell cycle-related pathways. Intriguingly, some differently expressed genes were noted in vascular development or coagulation function pathways.

CONCLUSION

We suggest that HIF1A-AS1 mediated the progression of thoracic aortic aneurysm by not only regulating the function of VSMCs, but also altering vascular development or coagulation function.

摘要

简介

胸主动脉瘤是一种具有强烈遗传贡献的潜在致命疾病。血管平滑肌细胞（VSMCs）的功能障碍导致了这种动脉瘤的形成。尽管先前的研究表明长非编码 RNA 缺氧诱导因子 1α-反义 RNA 1（HIF1A-AS1）在胸主动脉瘤的进展和发病机制中发挥了重要作用，但我们通过转录组学发现了 HIF1A-AS1 在 VSMCs 中的新调节机制。

方法

通过细胞计数试剂盒-8 检测细胞活力。通过 Annexin V-荧光素异硫氰酸酯/碘化丙啶双重染色评估细胞凋亡。Transwell 迁移实验和划痕愈合实验用于检查 HIF1A-AS1 对 VSMCs 迁移能力的影响。使用 NextSeq XTen 系统（Illumina）收集 RNA 测序数据。最后，逆转录-定量聚合酶链反应证实了 RNA 测序结果的准确性和可靠性。

结果

我们观察到过表达 HIF1A-AS1 成功地促进了 VSMCs 的凋亡，显著改变了细胞周期分布，并大大减弱了迁移，进一步强调了 HIF1A-AS1 对胸主动脉瘤的强大促进作用。此外，进行了转录组学以揭示其潜在机制。共鉴定出 175 个差异表达基因，其中一些基因富集在凋亡、迁移和细胞周期相关途径中。有趣的是，一些差异表达基因在血管发育或凝血功能途径中被注意到。

结论

我们认为，HIF1A-AS1 通过不仅调节 VSMCs 的功能，而且改变血管发育或凝血功能，介导胸主动脉瘤的进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96c0/10550220/cb4f87ffd55e/bjcvs-38-06-e20220260-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96c0/10550220/c3aceab66376/bjcvs-38-06-e20220260-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96c0/10550220/c45d0ebca00f/bjcvs-38-06-e20220260-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96c0/10550220/f5e17248cadd/bjcvs-38-06-e20220260-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96c0/10550220/63f0fdd0edb9/bjcvs-38-06-e20220260-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96c0/10550220/a1079171c286/bjcvs-38-06-e20220260-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96c0/10550220/cb4f87ffd55e/bjcvs-38-06-e20220260-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96c0/10550220/c3aceab66376/bjcvs-38-06-e20220260-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96c0/10550220/c45d0ebca00f/bjcvs-38-06-e20220260-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96c0/10550220/f5e17248cadd/bjcvs-38-06-e20220260-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96c0/10550220/63f0fdd0edb9/bjcvs-38-06-e20220260-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96c0/10550220/a1079171c286/bjcvs-38-06-e20220260-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96c0/10550220/cb4f87ffd55e/bjcvs-38-06-e20220260-g06.jpg

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