Suppr超能文献

血小板衍生的微泡分泌的 miR-191 通过抑制 CBS 诱导肾小管上皮细胞凋亡,并参与肾缺血再灌注损伤。

miR-191 secreted by platelet-derived microvesicles induced apoptosis of renal tubular epithelial cells and participated in renal ischemia-reperfusion injury via inhibiting CBS.

机构信息

a Department of Urology, Henan Provincial People's Hospital , People's Hospital of Zhengzhou University , Zhengzhou , China.

出版信息

Cell Cycle. 2019 Jan;18(2):119-129. doi: 10.1080/15384101.2018.1542900. Epub 2019 Jan 3.

Abstract

In this study, we aimed to reveal the role of miR-191 in apoptosis of renal tubular epithelial cells and in the involvement of renal ischemia-reperfusion injury. Renal transplantation rat model was established. miR-191 and Cystathionine-β-synthase (CBS) were measured by qRT-PCR and Western blot. The regulation of miR-191 on CBS was detected by luciferase reporter assay. We found miR-191 expression in platelets and platelet microvesicles (P-MVs) of patients and model rats was significantly upregulated than that of health and normal rats. Also, mRNA and protein levels of CBS in renal tissues of patients were significantly downregulated than that of health and normal rats. We also found that P-MVs could transfer miR-191 to HK-2 cells. Luciferase reporter assay showed that CBS was a direct target of miR-191. In addition, we proved that P-MVs-secreted miR-191 inhibited CBS expression in HK-2 cells, and P-MVs-secreted miR-191 promoted HK-2 cell apoptosis via CBS. Finally, we verified the trends of CBS expressions, HK-2 cell apoptosis and apoptosis-related proteins in vivo were similar as the trends in vitro. Therefore, CBS was a direct target of miR-191, and miR-191 could transfer to HK-2 cells via P-MVs to decrease the expression of CBS, thus to promote cell apoptosis and renal IR injury.

摘要

在这项研究中,我们旨在揭示 miR-191 在肾小管上皮细胞凋亡和肾缺血再灌注损伤中的作用。建立了肾移植大鼠模型。通过 qRT-PCR 和 Western blot 检测 miR-191 和胱硫醚-β-合酶 (CBS)。通过荧光素酶报告基因检测 miR-191 对 CBS 的调控。我们发现患者和模型大鼠血小板和血小板微囊泡 (P-MV) 中的 miR-191 表达明显高于健康和正常大鼠。此外,患者肾组织中 CBS 的 mRNA 和蛋白水平明显低于健康和正常大鼠。我们还发现 P-MV 可以将 miR-191 转染到 HK-2 细胞中。荧光素酶报告基因检测显示 CBS 是 miR-191 的直接靶标。此外,我们证明 P-MV 分泌的 miR-191 抑制 HK-2 细胞中的 CBS 表达,并且 P-MV 分泌的 miR-191 通过 CBS 促进 HK-2 细胞凋亡。最后,我们验证了 CBS 表达、HK-2 细胞凋亡和凋亡相关蛋白的体内趋势与体外趋势相似。因此,CBS 是 miR-191 的直接靶标,miR-191 可以通过 P-MV 转移到 HK-2 细胞中,降低 CBS 的表达,从而促进细胞凋亡和肾 IR 损伤。

相似文献

2
5
MEG3 aggravates hypoxia/reoxygenation induced apoptosis of renal tubular epithelial cells via the miR-129-5p/HMGB1 axis.
J Biochem Mol Toxicol. 2021 Feb;35(2):e22649. doi: 10.1002/jbt.22649. Epub 2020 Nov 11.
6
MiR-125b-5p is involved in oxygen and glucose deprivation injury in PC-12 cells via CBS/HS pathway.
Nitric Oxide. 2018 Aug 1;78:11-21. doi: 10.1016/j.niox.2018.05.004. Epub 2018 May 17.
8
Loss of the Protein Cystathionine β-Synthase During Kidney Injury Promotes Renal Tubulointerstitial Fibrosis.
Kidney Blood Press Res. 2017;42(3):428-443. doi: 10.1159/000479295. Epub 2017 Jul 27.

引用本文的文献

1
Frontier role of extracellular vesicles in kidney disease.
J Nanobiotechnology. 2024 Sep 20;22(1):583. doi: 10.1186/s12951-024-02852-3.
5
Identification of hub genes associated with acute kidney injury induced by renal ischemia-reperfusion injury in mice.
Front Physiol. 2022 Sep 29;13:951855. doi: 10.3389/fphys.2022.951855. eCollection 2022.
6
Emerging role of extracellular vesicles in kidney diseases.
Front Pharmacol. 2022 Sep 12;13:985030. doi: 10.3389/fphar.2022.985030. eCollection 2022.

本文引用的文献

2
Role of miR‑21 on vascular endothelial cells in the protective effect of renal delayed ischemic preconditioning.
Mol Med Rep. 2017 Sep;16(3):2627-2635. doi: 10.3892/mmr.2017.6870. Epub 2017 Jun 28.
7
Effects of Platelet-Rich Plasma (PRP) on a Model of Renal Ischemia-Reperfusion in Rats.
PLoS One. 2016 Aug 23;11(8):e0160703. doi: 10.1371/journal.pone.0160703. eCollection 2016.
9
Reperfusion injury and reactive oxygen species: The evolution of a concept.
Redox Biol. 2015 Dec;6:524-551. doi: 10.1016/j.redox.2015.08.020. Epub 2015 Oct 8.
10
Differentially expressed microRNAs in kidney biopsies from various subtypes of nephrotic children.
Exp Mol Pathol. 2015 Dec;99(3):590-5. doi: 10.1016/j.yexmp.2015.10.003. Epub 2015 Oct 19.

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验