评估冠心病患者外周血单核细胞中 SORT1 和 SESN1 基因的表达及氧化应激状态。

IF 1.9 Q3 GENETICS & HEREDITY BMC genomic data Pub Date : 2024-11-02 DOI:10.1186/s12863-024-01275-1
Tayebe Ghiasvand, Jamshid Karimi, Iraj Khodadadi, Amirhossein Yazdi, Salman Khazaei, Zahra Abedi Kichi, Seyed Kianoosh Hosseini
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引用次数: 0

摘要

背景:冠状动脉疾病(CAD)是导致全球死亡的重要原因。最近的研究表明,Sortilin1(SORT1)和 Sestrin1(SESN1)在脂质代谢中起着关键作用,并参与了冠状动脉疾病的发病。SORT1 的异常表达或活性可导致代谢和血管疾病。包括 SESN1 在内的胰蛋白酶通过维持新陈代谢平衡帮助细胞存活,同时还能减少氧化应激(OS)。氧化应激有助于动脉粥样硬化相关疾病(如冠状动脉粥样硬化)的发展。该研究旨在比较 CAD 患者和对照组外周血单核细胞(PBMCs)中 SORT1 和 SESN1 的基因表达以及血清 OS 标志物:病例对照研究包括 49 名 CAD 患者和 40 名对照组。采用 qRT-PCR 技术对 SORT1 和 SESN1 基因的表达进行量化,并通过 Western 印迹技术对 SORT1 蛋白的表达进行评估。采用分光光度法和荧光法测量了包括总氧化状态(TOS)、总抗氧化能力(TAC)和丙二醛(MDA)在内的 OS 标记物:结果:SORT1 基因和蛋白质的表达在不同组间相似。CAD患者的SESN1基因表达量下降不明显。MDA水平在CAD患者中明显升高,而TOS和TAC水平无明显差异:对于动脉粥样硬化相关疾病(如 CAD),MDA 显示出作为一种非侵入性、易于使用、经济实惠且稳定的生物标记物的潜力。要阐明 SORT1 和 SESN1 在 CAD 发病机制中的确切作用,还需要进一步的研究。
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Evaluating SORT1 and SESN1 genes expression in peripheral blood mononuclear cells and oxidative stress status in patients with coronary artery disease.

Background: Coronary artery disease (CAD) significantly contributes to global fatalities. Recent studies have demonstrated the crucial roles of sortilin1 (SORT1) and sestrin1 (SESN1) in lipid metabolism, as well as their involvement in the development of CAD. The aberrant expression or activity of SORT1 can consequently lead to metabolic and vascular diseases. Sestrins, including SESN1, play a crucial role in helping cells survive by maintaining metabolic balance while also reducing oxidative stress (OS). OS contributes to the progression of atherosclerosis-related diseases, such as CAD. The study aimed to compare the gene expression of SORT1 and SESN1 in peripheral blood mononuclear cells (PBMCs), alongside serum OS markers, in CAD patients and controls.

Materials: The case-control study included 49 CAD patients and 40 controls. The expression of the SORT1 and SESN1 genes was quantified using qRT-PCR, and the expression of the SORT1 protein was evaluated by western blotting. OS markers, including total oxidation status (TOS), total antioxidant capacity (TAC), and malondialdehyde (MDA), were measured using spectrophotometric and fluorometric methods.

Results: SORT1 gene and protein expressions were similar between groups. CAD patients had a non-significant decrease in SESN1 gene expression. MDA levels were significantly higher in CAD patients, whereas TOS and TAC levels did not differ significantly.

Conclusion: For atherosclerosis-related disorders like CAD, MDA shows potential as a non-invasive, easy-to-use, affordable, and stable biomarker. Further research is needed to elucidate the precise roles of SORT1 and SESN1 in CAD pathogenesis.

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