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微小RNA-24能否通过靶向YKL-40影响系统性红斑狼疮的心血管发病率?

Can Micro RNA-24 Affect the Cardiovascular Morbidity in Systemic Lupus Erythematosus by Targeting YKL-40?

作者信息

Alhelf Maha, Rashed Laila, Ahmed Sahar, Mady Mohamed, Abdelgwad Marwa

机构信息

Biotechnology School, Nile University, Giza, Egypt.

Medical Biochemistry and Molecular Biology Department, Faculty of Medicine, Cairo University, Cairo, Egypt.

出版信息

Rep Biochem Mol Biol. 2022 Oct;11(3):511-523. doi: 10.52547/rbmb.11.3.511.

Abstract

BACKGROUND

Systemic lupus erythematosus (SLE) is an autoimmune disease with inflammatory nature. One of the leading causes of death in SLE patients is cardiovascular (CVS) morbidity. MiRNA-24 is highly expressed in vascular endothelial cells (VECs). This dysregulated expression pattern is associated with dysfunction or even damage of VECs and leads to the occurrence of cardiovascular diseases. YKL- 40 is an inflammatory glycoprotein involved in the pathogenesis of endothelial dysfunction and thereby atherosclerosis. In this work, we aimed at illustrating the possible role of miR-24 and its target YKL-40 in the pathogenesis of the CVS morbidity associated with SLE.

METHODS

This work was conducted on 40 SLE patients and 40 healthy controls. Quantitative real-time PCR (qPCR) was done to estimate the expression level of miRNA-24 in serum. In addition, we measured the serum level of YKL-40 using ELISA.

RESULTS

miR-24-fold change was found to be down-regulated, whereas serum YKL- 40 was up-regulated among SLE patients with observed significant and negative correlation between the two parameters.

CONCLUSION

Our study provided an insight about the role of miR-24 and its target serum YKL-40 protein in the development of SLE-related inflammation and atherosclerosis.

摘要

背景

系统性红斑狼疮(SLE)是一种具有炎症性质的自身免疫性疾病。SLE患者主要死亡原因之一是心血管(CVS)疾病。MiRNA - 24在血管内皮细胞(VECs)中高表达。这种失调的表达模式与VECs功能障碍甚至损伤相关,并导致心血管疾病的发生。YKL - 40是一种炎症糖蛋白,参与内皮功能障碍及动脉粥样硬化的发病机制。在本研究中,我们旨在阐明miR - 24及其靶标YKL - 40在与SLE相关的CVS疾病发病机制中的可能作用。

方法

本研究对40例SLE患者和40例健康对照者进行。采用定量实时PCR(qPCR)检测血清中miRNA - 24的表达水平。此外,我们使用酶联免疫吸附测定(ELISA)法检测血清YKL - 40水平。

结果

发现SLE患者中miR - 24倍数变化下调,而血清YKL - 40上调,且这两个参数之间存在显著负相关。

结论

我们的研究揭示了miR - 24及其靶标血清YKL - 40蛋白在SLE相关炎症和动脉粥样硬化发展中的作用。

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