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微小病变性肾病综合征缓解和复发之间的 DNA 甲基化变化。

DNA methylation changes between relapse and remission of minimal change nephrotic syndrome.

机构信息

Department of Pediatrics, Gunma University Graduate School of Medicine, 3-39-22 Showa-machi, Maebashi, Gunma, 371-8511, Japan.

出版信息

Pediatr Nephrol. 2012 Dec;27(12):2233-41. doi: 10.1007/s00467-012-2248-z. Epub 2012 Aug 2.

DOI:10.1007/s00467-012-2248-z
PMID:22855301
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3491205/
Abstract

BACKGROUND

DNA methylation of gene promoters is associated with transcriptional inactivation. Changes in DNA methylation can lead to differences in gene expression levels and thereby influence disease development. We hypothesized that epigenetics underlies the pathogenesis of minimal change nephrotic syndrome (MCNS).

METHODS

Genome-wide DNA methylation changes between relapse and remission in monocytes (n = 6) and naive T helper cells (Th0s) (n = 4) isolated from patients with MCNS were investigated using the microarray-based integrated analysis of methylation by isochizomers (MIAMI) method. We confirmed the MIAMI results using bisulfite-pyrosequencing analysis. Expression analysis was performed using quantitative real-time PCR.

RESULTS

Three gene loci (GATA2, PBX4, and NYX) were significantly less methylated in Th0s during relapse than in remission, compared to none in monocytes. In addition, the distance distribution from the regression line of all probes in MIAMI was significantly different between monocytes and Th0s. The mRNA levels of the three genes in Th0s were not significantly different between relapse and remission.

CONCLUSIONS

Our results demonstrate that the change in DNA methylation patterns from remission to relapse in MCNS occurs predominantly in Th0s rather than in monocytes and suggest that epigenetic regulation in Th0s underlies the pathogenesis of MCNS.

摘要

背景

基因启动子的 DNA 甲基化与转录失活有关。DNA 甲基化的变化可导致基因表达水平的差异，从而影响疾病的发展。我们假设表观遗传学是微小病变性肾病综合征（MCNS）发病机制的基础。

方法

采用基于微阵列的等位基因特异性甲基化分析（MIAMI）方法，研究了从 MCNS 患者分离的单核细胞（n=6）和初始 T 辅助细胞（Th0）（n=4）中复发和缓解期之间的全基因组 DNA 甲基化变化。我们使用亚硫酸氢盐焦磷酸测序分析证实了 MIAMI 结果。采用实时定量 PCR 进行表达分析。

结果

与单核细胞相比，在复发期 Th0 中，有三个基因座（GATA2、PBX4 和 NYX）的甲基化明显低于缓解期，而单核细胞中无一例发生这种情况。此外，MIAMI 中所有探针的回归线之间的距离分布在单核细胞和 Th0 之间存在显著差异。Th0 中这三个基因的 mRNA 水平在复发和缓解之间没有显著差异。

结论

我们的研究结果表明，在 MCNS 中，从缓解到复发的 DNA 甲基化模式的变化主要发生在 Th0 中，而不是单核细胞中，这表明 Th0 中的表观遗传调控是 MCNS 发病机制的基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c3aa/3491205/c90bdc12885d/467_2012_2248_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c3aa/3491205/cbfbdb4e1c6e/467_2012_2248_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c3aa/3491205/267fae1ca71b/467_2012_2248_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c3aa/3491205/b584d51a2165/467_2012_2248_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c3aa/3491205/c90bdc12885d/467_2012_2248_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c3aa/3491205/cbfbdb4e1c6e/467_2012_2248_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c3aa/3491205/267fae1ca71b/467_2012_2248_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c3aa/3491205/b584d51a2165/467_2012_2248_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c3aa/3491205/c90bdc12885d/467_2012_2248_Fig4_HTML.jpg

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