lncRNA MALAT1在IgA血管炎性肾炎患儿中的表达及机制探讨
Expression and mechanism exploration of lncRNA MALAT1 in children with IgA vasculitis nephritis.
摘要(中文译文)
IgA血管炎（IgAV）是儿童最常见的全身性小血管炎。肾脏受累称为IgA血管炎肾炎（IgAVN），是该病最严重的并发症之一。本研究的主要目的是评估转移相关肺腺癌转录本1（MALAT1）在IgAVN中的异常表达，并通过调控miR-142-3p/SYK轴阐明其参与潜在致病机制的机制。采用逆转录定量聚合酶链反应（RT-qPCR）定量检测MALAT1表达水平。使用双荧光素酶报告基因实验验证MALAT1、miR-142-3p和SYK之间的靶向关系。通过CCK-8实验和凋亡标志物检测评估MALAT1和miR-142-3p对细胞增殖和凋亡的体外功能影响。同时，利用酶联免疫吸附实验（ELISA）分析炎症因子水平。MALAT1和SYK在IgAVN患者中显著上调，而miR-142-3p下调。MALAT1在区分IgAVN患者与无肾脏受累的IgAV患者方面表现出潜在价值。此外，敲低MALAT1可通过调控miR-142-3p/SYK轴抑制血管紧张素II（Ang II）诱导的人肾小球系膜细胞（HGMCs）过度增殖、促进凋亡并减轻炎症反应。MALAT1可能是IgAVN的生物标志物，MALAT1/miR-142-3p/SYK轴可能成为IgAVN的治疗靶点。
Abstract
IgA vasculitis (IgAV) is the most common systemic small vessel vasculitis in children. Renal involvement is called IgA vasculitis nephritis (IgAVN) and represents one of the most severe complications of this disease. The primary objective of this study was to evaluate the abnormal expression of Metastasis-Associated Lung Adenocarcinoma Transcript 1 (MALAT1) in IgAVN and to elucidate its involvement in the underlying pathogenic mechanisms by regulating the miR-142-3p/SYK axis. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was employed to quantify MALAT1 expression levels. A dual-luciferase reporter assay was used to verify the targeting relationships among MALAT1, miR-142-3p, and SYK. The in vitro functional effects of MALAT1 and miR-142-3p on cell proliferation and apoptosis were assessed using CCK-8 assays and detection of apoptotic markers. Simultaneously, an enzyme-linked immunosorbent assay (ELISA) was utilized to analyze the levels of inflammatory factors. MALAT1 and SYK were significantly upregulated in IgAVN patients, whereas miR-142-3p was downregulated. MALAT1 exhibited potential in distinguishing IgAVN patients from those with IgAV without renal involvement. Furthermore, knockdown of MALAT1 inhibited excessive proliferation, promoted apoptosis, and alleviated the inflammatory response of human glomerular mesangial cells (HGMCs) induced by angiotensin II (Ang II) through regulation of the miR-142-3p/SYK axis. MALAT1 may be a biomarker of IgAVN, and the MALAT1/miR-142-3p/SYK axis may become a therapeutic target for IgAVN.
如何引用
AMA
Shuo Chang, Yueyue Kan, Tian Zhang, Qin Zhang. Expression and mechanism exploration of lncRNA MALAT1 in children with IgA vasculitis nephritis.. Immunobiology. 2026; doi:10.1016/j.imbio.2026.153202.
APA
Shuo Chang, Yueyue Kan, Tian Zhang, Qin Zhang (2026). Expression and mechanism exploration of lncRNA MALAT1 in children with IgA vasculitis nephritis.. Immunobiology. https://doi.org/10.1016/j.imbio.2026.153202
GB/T 7714
Shuo Chang, Yueyue Kan, Tian Zhang, Qin Zhang. Expression and mechanism exploration of lncRNA MALAT1 in children with IgA vasculitis nephritis.[J]. Immunobiology, 2026 doi:10.1016/j.imbio.2026.153202.
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