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长链非编码 RNA TP73-AS1 通过靶向 miR-654-3p/AKT3 轴促进动脉粥样硬化中氧化型低密度脂蛋白诱导的内皮细胞凋亡。

LncRNA TP73-AS1 promotes oxidized low-density lipoprotein-induced apoptosis of endothelial cells in atherosclerosis by targeting the miR-654-3p/AKT3 axis.

机构信息

Stomatological Hospital, Southern Medical University, No. 366 Jiangnan Avenue South, Haizhu District, Guangzhou City, Guangdong Province, People's Republic of China.

Peking University School of Stomatology, Beijing, 100081, People's Republic of China.

出版信息

Cell Mol Biol Lett. 2021 Jun 8;26(1):27. doi: 10.1186/s11658-021-00264-x.

DOI:10.1186/s11658-021-00264-x
PMID:34103010
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8188714/
Abstract

BACKGROUND

Although lncRNA TP73-AS1 has been shown to play important roles in various human diseases, its function in atherosclerosis (AS) remains unclear.

METHODS

Human aortic endothelial cells (HAECs) were treated with 50 μg/ml oxidized low-density lipoprotein (ox-LDL) to establish an atherosclerotic cell model. The expression of TP73-AS1, miR-654-3p and AKT3 was detected by qRT-PCR. Cell functions were evaluated CCK-8 assay and flow cytometry. The protein levels of apoptosis-related proteins were evaluated by western blot. The binding relationship among TP73-AS1, miR-654-3p and AKT3 was determined by bioinformatics analysis and luciferase reporter assay.

RESULTS

TP73-AS1 was upregulated and miR-654-3p was downregulated in ox-LDL treated HAECs. TP73-AS1 silencing and miR-654-3p mimics decreased the viability and inhibited apoptosis of ox-LDL treated HAECs, decreased the expression levels of c-caspase-9, c-caspase-3 and Bax, and increased Bcl-2 expression. In addition, miR-654-3p inhibitor significantly reversed the inhibitory effects of si-TP73-AS1 on cell viability and apoptosis. TP73-AS1 could positively regulate AKT3 through directly sponging miR-654-3p.

CONCLUSION

TP73-AS1 promoted apoptosis of ox-LDL stimulated endothelial cells by targeting the miR-654-3p/AKT3 axis, suggesting that TP73-AS1 might be a potential target for AS treatment.

摘要

背景

尽管长链非编码 RNA TP73-AS1 在各种人类疾病中发挥着重要作用，但它在动脉粥样硬化（AS）中的功能仍不清楚。

方法

用 50μg/ml 氧化型低密度脂蛋白（ox-LDL）处理人主动脉内皮细胞（HAECs），建立动脉粥样硬化细胞模型。采用 qRT-PCR 检测 TP73-AS1、miR-654-3p 和 AKT3 的表达。采用 CCK-8 法和流式细胞术检测细胞功能。采用 Western blot 检测凋亡相关蛋白的蛋白水平。通过生物信息学分析和荧光素酶报告实验确定 TP73-AS1、miR-654-3p 和 AKT3 之间的结合关系。

结果

ox-LDL 处理的 HAECs 中 TP73-AS1 上调，miR-654-3p 下调。TP73-AS1 沉默和 miR-654-3p 模拟物降低了 ox-LDL 处理的 HAECs 的活力并抑制了其凋亡，降低了 c-caspase-9、c-caspase-3 和 Bax 的表达水平，并增加了 Bcl-2 的表达。此外，miR-654-3p 抑制剂显著逆转了 si-TP73-AS1 对细胞活力和凋亡的抑制作用。TP73-AS1 可以通过直接海绵 miR-654-3p 正向调节 AKT3。

结论

TP73-AS1 通过靶向 miR-654-3p/AKT3 轴促进 ox-LDL 刺激的内皮细胞凋亡，提示 TP73-AS1 可能是 AS 治疗的潜在靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86bc/8188714/25274cf2e5d6/11658_2021_264_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86bc/8188714/c79975057264/11658_2021_264_Fig1_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86bc/8188714/ceed12550c9d/11658_2021_264_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86bc/8188714/f2bd4299f548/11658_2021_264_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86bc/8188714/25274cf2e5d6/11658_2021_264_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86bc/8188714/c79975057264/11658_2021_264_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86bc/8188714/52c882e44275/11658_2021_264_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86bc/8188714/a8a95c201c47/11658_2021_264_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86bc/8188714/4428629783a2/11658_2021_264_Fig4_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86bc/8188714/f2bd4299f548/11658_2021_264_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86bc/8188714/25274cf2e5d6/11658_2021_264_Fig7_HTML.jpg

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