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长链非编码RNA IFNG-AS1和TH2LCRR作为糖尿病肾病中Th1/Th2失衡的潜在生物标志物：从生物信息学到实验验证

LncRNAs IFNG-AS1 and TH2LCRR as potential biomarkers of Th1/Th2 imbalance in diabetic nephropathy: From bioinformatics to experimental validation.

作者信息

Hosseini Seyed Amir Hossein, Ajorlou Parisa, Salehian Maryam, Dehghani Aghdas

机构信息

Endocrinology and Metabolism Research Center, Hormozgan University of Medical Sciences, Bandar Abbas, Iran.

Department of Medical Genetics, Faculty of Medicine, Hormozgan University of Medical Sciences, Bandar Abbas, Iran.

出版信息

Biochem Biophys Rep. 2025 Jun 14;43:102093. doi: 10.1016/j.bbrep.2025.102093. eCollection 2025 Sep.

DOI:10.1016/j.bbrep.2025.102093
PMID:40937328
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12420516/
Abstract

BACKGROUND

The inflammatory response is a pivotal mechanism underlying the progression of type 2 diabetes mellitus (T2DM) into diabetic nephropathy (DN). Upstream lncRNAs regulate inflammatory molecules, and their dysregulation can disrupt immune homeostasis. Th1/Th2 imbalance is one of the most significant causes of DN progression. This research aims to uncover novel biomarkers and elucidate the underlying molecular mechanisms involved in DN.

METHODS

The GSE135390 dataset was analyzed to identify differentially expressed genes (DEGs) associated with Th1 cell differentiation. Based on literature review and NcPath databases, IFNG-AS1(Th1) and TH2LCRR (Th2) were selected as the top lncRNAs. To validate our bioinformatics findings, real-time PCR was conducted on 90 participants categorized into four groups: 30 with T2DM, 30 with DN (15 with microalbuminuria and 15 with ESRD), and 30 healthy controls.

RESULTS

The analysis of real-time PCR results revealed a notable upregulation in IFNG-AS1 expression in ESRD patients compared to individuals with T2DM and healthy controls. Moreover, a significant increase in IFNG-AS1 expression was observed in patients with microalbuminuria relative to healthy subjects. Conversely, TH2LCRR expression was notably reduced in patients with ESRD, microalbuminuria, and T2DM compared to healthy individuals. Expression of IFNG-AS1 and TH2LCRR showed strong correlation with biochemical markers, including HbA1c, ESR, BUN, GFR, and albumin.

CONCLUSION

This study demonstrates the potential role of IFNG-AS1 and TH2LCRR as key regulators in the immunopathogenesis of DN. Their dysregulated expression may contribute to Th1/Th2 imbalance, providing a deeper understanding of immune-mediated mechanisms involved in DN progression.

摘要

背景

炎症反应是2型糖尿病（T2DM）进展为糖尿病肾病（DN）的关键机制。上游长链非编码RNA（lncRNAs）调节炎症分子，其失调会破坏免疫稳态。Th1/Th2失衡是DN进展的最重要原因之一。本研究旨在发现新的生物标志物，并阐明DN潜在的分子机制。

方法

分析GSE135390数据集，以鉴定与Th1细胞分化相关的差异表达基因（DEGs）。基于文献综述和NcPath数据库，选择IFNG-AS1（Th1）和TH2LCRR（Th2）作为排名靠前的lncRNAs。为验证我们的生物信息学研究结果，对90名参与者进行了实时PCR检测，这些参与者分为四组：30名T2DM患者、30名DN患者（15名微量白蛋白尿患者和15名终末期肾病患者）以及30名健康对照者。

结果

实时PCR结果分析显示，与T2DM患者和健康对照者相比，终末期肾病患者中IFNG-AS1表达显著上调。此外，与健康受试者相比，微量白蛋白尿患者中IFNG-AS1表达显著增加。相反，与健康个体相比，终末期肾病、微量白蛋白尿和T2DM患者中TH2LCRR表达显著降低。IFNG-AS1和TH2LCRR的表达与生化标志物，包括糖化血红蛋白、红细胞沉降率、血尿素氮、肾小球滤过率和白蛋白，显示出强相关性。

结论

本研究证明了IFNG-AS1和TH2LCRR作为DN免疫发病机制关键调节因子的潜在作用。它们的失调表达可能导致Th1/Th2失衡，从而更深入地了解DN进展中涉及的免疫介导机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b139/12420516/be2a5ff87c8a/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b139/12420516/86feaa7b355d/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b139/12420516/3309df799ae0/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b139/12420516/e7a20c6fda2a/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b139/12420516/fc766cd678a6/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b139/12420516/8f66c456240b/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b139/12420516/be2a5ff87c8a/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b139/12420516/86feaa7b355d/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b139/12420516/3309df799ae0/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b139/12420516/e7a20c6fda2a/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b139/12420516/fc766cd678a6/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b139/12420516/8f66c456240b/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b139/12420516/be2a5ff87c8a/gr5.jpg

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