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高磷刺激内皮细胞外囊泡的 RNA-seq 分析为血管钙化的发生机制提供了新视角。

RNA-seq analysis of extracellular vesicles from hyperphosphatemia-stimulated endothelial cells provides insight into the mechanism underlying vascular calcification.

机构信息

The First Affiliated Hospital, Department of Gastroenterology, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, China.

The First Affiliated Hospital, Department of Nephrology, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, China.

出版信息

BMC Nephrol. 2022 May 21;23(1):192. doi: 10.1186/s12882-022-02823-6.

DOI:10.1186/s12882-022-02823-6
PMID:35597927
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9123672/
Abstract

BACKGROUND

Hyperphosphatemia (HP) is associated with vascular calcification (VC) in chronic kidney disease (CKD). However, relationship between HP-induced-endothelial extracellular vesicles (HP-EC-EVs) and VC is unclear, and miR expression in HP-EC-EVs has not been determined.

METHODS

We isolated HP-EC-EVs from endothelial cells with HP and observed that HP-EC-EVs were up-taken by vascular smooth muscle cells (VSMCs). HP-EC-EVs inducing calcium deposition was characterized by Alizarin Red S, colourimetric analysis and ALP activity. To investigate the mechanism of HP-EC-EVs-induced VSMC calcification, RNA-sequencing for HP-EC-EVs was performed.

RESULTS

We first demonstrated that HP-EC-EVs induced VSMC calcification in vitro. RNA-seq analysis of HP-EC-EVs illustrated that one known miR (hsa-miR-3182) was statistically up-regulated and twelve miRs were significantly down-regulated, which was verified by qRT-PCR. We predicted 58,209 and 74,469 target genes for those down- and up-regulated miRs respectively through miRDB, miRWalk and miRanda databases. GO terms showed that down- and up-regulated targets were mostly enriched in calcium-dependent cell-cell adhesion via plama membrane cell-adhesion molecules (GO:0,016,338, BP) and cell adhesion (GO:0,007,155, BP), plasma membrane (GO:0,005,886, CC), and metal ion binding (GO:0,046,914, MF) and ATP binding (GO:0,005,524, MF) respectively. Top-20 pathways by KEGG analysis included calcium signaling pathway, cAMP signaling pathway, and ABC transporters, which were closely related to VC.

CONCLUSION

Our results indicated that those significantly altered miRs, which were packaged in HP-EC-EVs, may play an important role in VC by regulating related pathways. It may provide novel insight into the mechanism of CKD calcification.

摘要

背景

高磷血症（HP）与慢性肾脏病（CKD）中的血管钙化（VC）有关。然而，HP 诱导的内皮细胞外囊泡（HP-EC-EVs）与 VC 之间的关系尚不清楚，并且 HP-EC-EVs 中的 miR 表达也尚未确定。

方法

我们从 HP 诱导的内皮细胞中分离出 HP-EC-EVs，并观察到 HP-EC-EVs 被血管平滑肌细胞（VSMCs）摄取。通过茜素红 S、比色分析和 ALP 活性来表征 HP-EC-EVs 诱导的钙沉积。为了研究 HP-EC-EVs 诱导的 VSMC 钙化的机制，我们对 HP-EC-EVs 进行了 RNA 测序。

结果

我们首先证明了 HP-EC-EVs 可在体外诱导 VSMC 钙化。HP-EC-EVs 的 RNA-seq 分析表明，一种已知的 miR（hsa-miR-3182）在统计学上被上调，而 12 个 miR 则显著下调，这通过 qRT-PCR 得到了验证。通过 miRDB、miRWalk 和 miRanda 数据库，我们预测了这些下调和上调 miR 的 58,209 和 74,469 个靶基因。GO 术语表明，下调和上调的靶基因主要富集在通过质膜细胞粘附分子的钙依赖性细胞-细胞粘附（GO：0.016.338，BP）和细胞粘附（GO：0.007.155，BP）、质膜（GO：0.005.886，CC）和金属离子结合（GO：0.046.914，MF）和 ATP 结合（GO：0.005.524，MF）。KEGG 分析的前 20 条途径包括钙信号通路、cAMP 信号通路和 ABC 转运体，这些途径与 VC 密切相关。

结论

我们的结果表明，那些被 HP-EC-EVs 包裹的明显改变的 miR 可能通过调节相关途径在 VC 中发挥重要作用。这可能为 CKD 钙化的机制提供新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0144/9123672/2fe132e93bf3/12882_2022_2823_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0144/9123672/d80d83cd046c/12882_2022_2823_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0144/9123672/76267831118e/12882_2022_2823_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0144/9123672/b164f32ece26/12882_2022_2823_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0144/9123672/2525c4cf32ce/12882_2022_2823_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0144/9123672/4d2372e7e3ae/12882_2022_2823_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0144/9123672/2f4081a5fa00/12882_2022_2823_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0144/9123672/2fe132e93bf3/12882_2022_2823_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0144/9123672/d80d83cd046c/12882_2022_2823_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0144/9123672/76267831118e/12882_2022_2823_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0144/9123672/b164f32ece26/12882_2022_2823_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0144/9123672/2525c4cf32ce/12882_2022_2823_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0144/9123672/4d2372e7e3ae/12882_2022_2823_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0144/9123672/2f4081a5fa00/12882_2022_2823_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0144/9123672/2fe132e93bf3/12882_2022_2823_Fig7_HTML.jpg

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