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LINC00265作为急性缺血性中风的诊断和预后标志物,并通过miR-155-5p/TRIM32轴抑制疾病进展。

LINC00265 Serves as a Diagnostic and Prognostic Marker for Acute Ischemic Stroke and INHIBITS Disease Progression Through the miR- 155 - 5p/TRIM32 Axis.

作者信息

Lv Zhicheng, Xie Xiaoming

机构信息

Department of Neurosurgery, The First People's Hospital of Chenzhou, Chenzhou, 423000, China.

Department of Neurosurgery Ward II, Changde Hospital, Xiangya School of Medicine, Central South University (The First People's Hospital of Changde City), No. 818, Renmin Road, Changde, 415000, China.

出版信息

Mol Neurobiol. 2025 May 3. doi: 10.1007/s12035-025-04973-8.

Abstract

Acute ischemic stroke (AIS) is a medical emergency stemming from a reduction in cerebral blood supply, leading to neuronal injury. LINC00265 may emerge as a highly promising biomarker for stroke. The aim of this investigation was to investigate the clinical and prognostic significance of LINC00265 in AIS, as well as to elucidate the molecular mechanisms through which LINC00265 influences AIS. Blood samples were collected from 131 AIS patients. qRT-PCR was employed to measure the expression levels of LINC00265. The diagnostic and prognostic value of LINC00265 were evaluated using ROC curve and Kaplan-Meier survival curves, respectively. To establish an in vitro model of AIS, HCMIEC/D3 cells were subjected to OGD/R treatment. Cell proliferation was assessed using CCK-8 assay. The concentrations of TNF-α, IL-6, IL-1β, IL-4, and IL-10 were measured using ELISA kit. The protein expression levels of VCAM-1 and ICAM-1 were detected by Western blot analysis. The expression of LINC00265 was found to be significantly downregulated in AIS patients and strongly correlated with disease severity. The reduced expression of LINC00265 exhibited considerable significance for both diagnosis and prognosis prediction of AIS. At the mechanistic level, LINC00265 mitigated OGD/R-induced cellular injury by modulating the miR-155-5p/TRIM32 axis. Therefore, overexpression of LINC00265 may potentially suppress disease progression in AIS by regulating miR-155-5p/TRIM32 axis.

摘要

急性缺血性卒中(AIS)是一种因脑供血减少导致神经元损伤的医疗急症。LINC00265可能成为一种极具前景的卒中生物标志物。本研究旨在探讨LINC00265在AIS中的临床及预后意义,并阐明LINC00265影响AIS的分子机制。收集了131例AIS患者的血样。采用qRT-PCR检测LINC00265的表达水平。分别使用ROC曲线和Kaplan-Meier生存曲线评估LINC00265的诊断和预后价值。为建立AIS体外模型,对HCMIEC/D3细胞进行氧糖剥夺/复氧(OGD/R)处理。使用CCK-8法评估细胞增殖。采用ELISA试剂盒检测肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)、白细胞介素-1β(IL-1β)、白细胞介素-4(IL-4)和白细胞介素-10(IL-10)的浓度。通过蛋白质免疫印迹分析检测血管细胞黏附分子-1(VCAM-1)和细胞间黏附分子-1(ICAM-1)的蛋白表达水平。研究发现,AIS患者中LINC00265的表达显著下调,且与疾病严重程度密切相关。LINC00265表达降低对AIS的诊断和预后预测均具有重要意义。在机制层面,LINC00265通过调节miR-155-5p/TRIM32轴减轻OGD/R诱导的细胞损伤。因此,LINC00265的过表达可能通过调节miR-155-5p/TRIM32轴抑制AIS的疾病进展。

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