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Inc-ITSN1-2 循环水平的纵向变化:一种反映急性缺血性脑卒中患者疾病严重程度、炎症、复发和死亡风险的新型生物标志物。

Longitudinal variation of circulating Inc-ITSN1-2: A novel biomarker reflecting disease severity, inflammation, recurrence, and death risk in acute ischemic stroke patients.

机构信息

Department of Neurology, The First Affiliated Hospital of Hebei North University, Zhangjiakou, China.

Department of ICU, The First Affiliated Hospital of Hebei North University, Zhangjiakou, China.

出版信息

J Clin Lab Anal. 2022 Jun;36(6):e24468. doi: 10.1002/jcla.24468. Epub 2022 May 2.

DOI:10.1002/jcla.24468
PMID:35500161
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9169226/
Abstract

BACKGROUND

Long noncoding RNA intersectin 1-2 (lnc-ITSN1-2) regulates inflammation and neuronal apoptosis; meanwhile, the latter two factors participate in the pathogenesis of acute ischemic stroke (AIS). Therefore, this study detected lnc-ITSN1-2 at multiple time points, aiming to explore its longitudinal variation and clinical value in the management of AIS patients.

METHODS

The current study enrolled 102 AIS patients, then detected their lnc-ITSN1-2 in peripheral blood mononuclear cell (PBMC) at baseline (D0), day (D)1, D3, D7, month (M)1, M3, M6, and year (Y)1 after admission using RT-qPCR. Additionally, lnc-ITSN1-2 in PBMC of 50 controls was also detected.

RESULTS

Lnc-ITSN1-2 was up-regulated in AIS patients than that in controls (p < 0.001). Lnc-ITSN1-2 positively associated with NIHSS score, TNF-α, and IL-17A (all p < 0.050) but was not linked with IL-6 (p = 0.093) in AIS patients. Notably, lnc-ITSN1-2 was gradually increased from D0 to D3; while it switched to decrease from D3 to Y1 in AIS patients. Lnc-ITSN1-2 disclosed similar longitudinal variation during 1 year in non-recurrent (p < 0.001), recurrent (p = 0.001), and survived patients (p < 0.001), while the variation of lnc-ITSN1-2 in died patients was not obvious (p = 0.132). More importantly, lnc-ITSN1-2 at D0, D3, D7, M1, M3, M6, and Y1 was higher in recurrent AIS patients than that in non-recurrent AIS patients (all p < 0.050); moreover, lnc-ITSN1-2 at D3, D7, M1, M3, and M6 was up-regulated in died AIS patients than AIS survivors (all p < 0.050).

CONCLUSION

The dynamic variation of Inc-ITSN1-2 could serve as a biomarker reflecting disease severity, inflammatory cytokines, recurrence, and death risk in AIS patients.

摘要

背景

长链非编码 RNA intersectin 1-2(lnc-ITSN1-2)调节炎症和神经元凋亡;同时,后两者因素参与急性缺血性脑卒中(AIS)的发病机制。因此,本研究在多个时间点检测 lnc-ITSN1-2,旨在探讨其在 AIS 患者管理中的纵向变化和临床价值。

方法

本研究纳入 102 例 AIS 患者,然后使用 RT-qPCR 在基线(D0)、第 1 天(D1)、第 3 天(D3)、第 7 天(D7)、第 1 个月(M1)、第 3 个月(M3)、第 6 个月(M6)和第 1 年(Y1)时检测其外周血单核细胞(PBMC)中的 lnc-ITSN1-2。此外,还检测了 50 名对照者 PBMC 中的 lnc-ITSN1-2。

结果

AIS 患者的 lnc-ITSN1-2 高于对照组(p<0.001)。AIS 患者中,lnc-ITSN1-2 与 NIHSS 评分、TNF-α 和 IL-17A 呈正相关(均 p<0.050),但与 IL-6 无相关性(p=0.093)。值得注意的是,lnc-ITSN1-2 在 AIS 患者中从 D0 到 D3 逐渐升高,从 D3 到 Y1 则呈下降趋势。在非复发(p<0.001)、复发(p=0.001)和存活(p<0.001)患者中,lnc-ITSN1-2 在 1 年内也呈现出相似的纵向变化,而在死亡患者中(p=0.132),lnc-ITSN1-2 的变化并不明显。更重要的是,复发 AIS 患者在 D0、D3、D7、M1、M3、M6 和 Y1 时的 lnc-ITSN1-2 均高于非复发 AIS 患者(均 p<0.050),而在死亡 AIS 患者中,在 D3、D7、M1、M3 和 M6 时的 lnc-ITSN1-2 均高于 AIS 存活者(均 p<0.050)。

结论

lnc-ITSN1-2 的动态变化可作为反映 AIS 患者疾病严重程度、炎症细胞因子、复发和死亡风险的生物标志物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cdd5/9169226/56db9e83d9ba/JCLA-36-e24468-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cdd5/9169226/540146dd5d98/JCLA-36-e24468-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cdd5/9169226/b44151bf107d/JCLA-36-e24468-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cdd5/9169226/d249c28d2920/JCLA-36-e24468-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cdd5/9169226/68552677253d/JCLA-36-e24468-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cdd5/9169226/84812ec9d2a3/JCLA-36-e24468-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cdd5/9169226/56db9e83d9ba/JCLA-36-e24468-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cdd5/9169226/540146dd5d98/JCLA-36-e24468-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cdd5/9169226/b44151bf107d/JCLA-36-e24468-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cdd5/9169226/d249c28d2920/JCLA-36-e24468-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cdd5/9169226/68552677253d/JCLA-36-e24468-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cdd5/9169226/84812ec9d2a3/JCLA-36-e24468-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cdd5/9169226/56db9e83d9ba/JCLA-36-e24468-g006.jpg

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