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冠状动脉慢血流中的差异基因表达和 miRNA 调控网络。

Differential gene expression and miRNA regulatory network in coronary slow flow.

机构信息

Department of Cardiology, Zhongshan Boai Hospital Affiliated to South Medical University, No. 6, Chenggui Road, Zhongshan, 528405, Guangdong, China.

Department of Cardiology, The Fifth Affiliated Hospital of Xinjiang Medical University, No. 118 Henan West Road, Xinshi District, Urumqi, 830000, Xinjiang, China.

出版信息

Sci Rep. 2024 Apr 10;14(1):8419. doi: 10.1038/s41598-024-58745-w.

DOI:10.1038/s41598-024-58745-w
PMID:38600259
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11006858/
Abstract

Coronary slow flow (CSF) is characterized by slow progression of coronary angiography without epicardial stenosis. The aim of this study was to explore the potential biomarkers and regulatory mechanism for CSF. Peripheral blood mononuclear cells from 3 cases of CSF and 3 healthy controls were collected for high-throughput sequencing of mRNA and miRNA, respectively. The differentially expressed mRNAs (DE-mRNAs) and miRNAs (DE-miRNAs) was identified. A total of 117 DE-mRNAs and 32 DE-miRNAs were obtained and they were mainly enriched in immune and inflammatory responses. Twenty-six DE-mRNAs were the predicted target genes for miRNAs by RAID, and then the regulatory network of 15 miRNAs were constructed. In addition, through the PPI network, we identified the three genes (FPR1, FPR2 and CXCR4) with larger degrees as hub genes. Among them, FPR1 was regulated by hsa-miR-342-3p, hsa-let-7c-5p and hsa-miR-197-3p and participated in the immune response. Finally, we validated the differential expression of hub genes and key miRNAs between 20 CSF and 20 control. Moreover, we found that miR-342-3p has a targeted regulatory relationship with FPR1, and their expression is negatively correlated. Then we established a hypoxia/reoxygenation (H/R) HUVEC model and detected FPR1, cell proliferation and apoptosis. Transfection with miR-342-3p mimics can significantly promote the proliferation of HUVEC under H/R conditions. FPR1 were associated with CSF as a biomarker and may be regulated by miR-342-3p potential biomarkers.

摘要

冠状动脉慢血流（CSF）的特征是冠状动脉造影进展缓慢，而无外膜狭窄。本研究旨在探讨 CSF 的潜在生物标志物和调控机制。收集 3 例 CSF 和 3 例健康对照者的外周血单个核细胞，分别进行 mRNA 和 miRNA 的高通量测序。鉴定差异表达的 mRNAs（DE-mRNAs）和 miRNAs（DE-miRNAs）。共获得 117 个 DE-mRNAs 和 32 个 DE-miRNAs，主要富集于免疫和炎症反应。通过 RAID 预测到 26 个 DE-mRNAs 是 miRNA 的预测靶基因，然后构建了 15 个 miRNA 的调控网络。此外，通过 PPI 网络，我们确定了三个具有较大度数的基因（FPR1、FPR2 和 CXCR4）作为枢纽基因。其中，FPR1 受 hsa-miR-342-3p、hsa-let-7c-5p 和 hsa-miR-197-3p 的调控，参与免疫反应。最后，我们验证了 20 例 CSF 与 20 例对照之间枢纽基因和关键 miRNA 的差异表达。此外，我们发现 miR-342-3p 与 FPR1 具有靶向调控关系，且表达呈负相关。然后我们建立了缺氧/复氧（H/R）HUVEC 模型，并检测了 FPR1、细胞增殖和凋亡。转染 miR-342-3p 模拟物可显著促进 H/R 条件下 HUVEC 的增殖。FPR1 作为 CSF 的生物标志物与 CSF 相关，可能受 miR-342-3p 的调控。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd23/11006858/7302c9307281/41598_2024_58745_Fig9_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd23/11006858/7e548f0614af/41598_2024_58745_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd23/11006858/7302c9307281/41598_2024_58745_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd23/11006858/8e2d61da6354/41598_2024_58745_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd23/11006858/5f862759ba91/41598_2024_58745_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd23/11006858/33a6d40de2db/41598_2024_58745_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd23/11006858/475bc8eb4dba/41598_2024_58745_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd23/11006858/2f8f85480a6a/41598_2024_58745_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd23/11006858/0063cf542c16/41598_2024_58745_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd23/11006858/2e560a0c092b/41598_2024_58745_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd23/11006858/7e548f0614af/41598_2024_58745_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd23/11006858/7302c9307281/41598_2024_58745_Fig9_HTML.jpg

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