Long noncoding RNA ANRIL alleviates hypoxia-induced pulmonary microvascular endothelial cell damage

IF 4.4 3区医学 Q1 MEDICINE, GENERAL & INTERNAL European Journal of Clinical Investigation Pub Date : 2024-03-30 DOI:10.1111/eci.14202

Yijin Qi, Mingyue Chen, Tianyi Zhang, Beibei Zhao, Tianbo Jin, Dongya Yuan

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Abstract

Background

High-altitude pulmonary oedema (HAPE) is a form of noncardiogenic pulmonary oedema. Studies have found that long noncoding RNA (lncRNA) plays an important role in HAPE. ANRIL is significant in pulmonary illnesses, which implies that alterations in ANRIL expression levels may be involved in the beginning and development of HAPE. However, the specific mechanism is indistinct. The present study is meant to explore the effect and mechanism of ANRIL on hypoxic-induced injury of pulmonary microvascular endothelial cells (PMEVCs).

Methods

In the hypoxic model of PMVECs, overexpression of ANRIL or knockdown of miR-181c-5p was performed to assess cell proliferation, apoptosis, and migration. Furthermore, the levels of apoptosis-related proteins, inflammatory factors, and vascular active factors were also measured.

Results

The results showed that, after 24 h of hypoxia, PMVECs proliferation and migration were suppressed in comparison to the control group, along with an increase in apoptosis, a decrease in the expression of ANRIL, and an increase in the expression of miR-181c-5p (all p < .05). The damage caused by hypoxia in PMVECs can be lessened by overexpressing ANRIL, which also inhibits the production of TNF-α, iNOS, and VEGF as well as BAX and cleaved caspase-3 (all p < .05). Further experimental results showed that overexpression of ANRIL and knockdown of miR-181c-5p had the same protection against hypoxic injury in PMVECs (all p < .05).

Conclusions

Our study suggests that ANRIL may prevent hypoxia injury to PMVECs in HAPE through the negative regulation of miR-181c-5p.

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长非编码 RNA ANRIL 可减轻缺氧诱导的肺微血管内皮细胞损伤

背景：高海拔肺水肿（HAPE）是一种非心源性肺水肿：高海拔肺水肿（HAPE）是一种非心源性肺水肿。研究发现，长非编码 RNA（lncRNA）在 HAPE 中起着重要作用。ANRIL 在肺部疾病中具有重要作用，这意味着 ANRIL 表达水平的改变可能与 HAPE 的开始和发展有关。然而，具体机制尚不明确。本研究旨在探讨ANRIL对缺氧诱导的肺微血管内皮细胞（PMEVCs）损伤的影响和机制：方法：在肺微血管内皮细胞缺氧模型中，过表达 ANRIL 或敲除 miR-181c-5p，以评估细胞增殖、凋亡和迁移。此外，还测定了细胞凋亡相关蛋白、炎症因子和血管活性因子的水平：结果表明：与对照组相比，缺氧 24 小时后，PMVECs 的增殖和迁移受到抑制，同时细胞凋亡增加，ANRIL 的表达减少，miR-181c-5p 的表达增加（均为 p）：我们的研究表明，ANRIL 可通过负调控 miR-181c-5p 防止 HAPE 中 PMVECs 的缺氧损伤。

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来源期刊

European Journal of Clinical Investigation 医学-医学：内科

CiteScore

9.50

自引率

3.60%

发文量

192

审稿时长

1 months

期刊介绍： EJCI considers any original contribution from the most sophisticated basic molecular sciences to applied clinical and translational research and evidence-based medicine across a broad range of subspecialties. The EJCI publishes reports of high-quality research that pertain to the genetic, molecular, cellular, or physiological basis of human biology and disease, as well as research that addresses prevalence, diagnosis, course, treatment, and prevention of disease. We are primarily interested in studies directly pertinent to humans, but submission of robust in vitro and animal work is also encouraged. Interdisciplinary work and research using innovative methods and combinations of laboratory, clinical, and epidemiological methodologies and techniques is of great interest to the journal. Several categories of manuscripts (for detailed description see below) are considered: editorials, original articles (also including randomized clinical trials, systematic reviews and meta-analyses), reviews (narrative reviews), opinion articles (including debates, perspectives and commentaries); and letters to the Editor.