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

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          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.

          Electronic supplementary material

          The online version of this article (doi:10.1007/s00467-012-2248-z) contains supplementary material, which is available to authorized users.

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          Most cited references30

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          Role for DNA methylation in genomic imprinting.

          E Li, C. Beard, R Jaenisch (1993)
          The paternal and maternal genomes are not equivalent and both are required for mammalian development. The difference between the parental genomes is believed to be due to gamete-specific differential modification, a process known as genomic imprinting. The study of transgene methylation has shown that methylation patterns can be inherited in a parent-of-origin-specific manner, suggesting that DNA methylation may play a role in genomic imprinting. The functional significance of DNA methylation in genomic imprinting was strengthened by the recent finding that CpG islands (or sites) in three imprinted genes, H19, insulin-like growth factor 2 (Igf-2), and Igf-2 receptor (Igf-2r), are differentially methylated depending on their parental origin. We have examined the expression of these three imprinted genes in mutant mice that are deficient in DNA methyltransferase activity. We report here that expression of all three genes was affected in mutant embryos: the normally silent paternal allele of the H19 gene was activated, whereas the normally active paternal allele of the Igf-2 gene and the active maternal allele of the Igf-2r gene were repressed. Our results demonstrate that a normal level of DNA methylation is required for controlling differential expression of the paternal and maternal alleles of imprinted genes.
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            Pathogenesis of lipoid nephrosis: a disorder of T-cell function.

            J Shalhoub (1974)
            Clinical observations suggest that lipoid nephrosis is produced by a systemic abnormality of T-cell function resulting in the secretion of a circulating chemical mediator toxic to an immunologically innocent glomerular basement membrane. The lack of evidence of a humoral antibody response, remission induced by measles which modifies cell-mediated immunity, the therapeutic benefits of steroids and cyclophosphamide which also abate cell-mediated responses, and the occurrence of this syndrome in Hodgkin's disease support this hypothesis. The susceptibility of untreated patients to pneumococcal infections may be of primary or secondary pathogenetic importance. Taken together, the data suggest that this syndrome is a clinical expression of a self-limited primary immune-deficiency disease.
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              Beyond Watson and Crick: DNA methylation and molecular enzymology of DNA methyltransferases.

              Albert Jeltsch (2002)
              DNA methyltransferases catalyze the transfer of a methyl group from S-adenosyl-L-methionine to cytosine or adenine bases in DNA. These enzymes challenge the Watson/Crick dogma in two instances: 1) They attach inheritable information to the DNA that is not encoded in the nucleotide sequence. This so-called epigenetic information has many important biological functions. In prokaryotes, DNA methylation is used to coordinate DNA replication and the cell cycle, to direct postreplicative mismatch repair, and to distinguish self and nonself DNA. In eukaryotes, DNA methylation contributes to the control of gene expression, the protection of the genome against selfish DNA, maintenance of genome integrity, parental imprinting, X-chromosome inactivation in mammals, and regulation of development. 2) The enzymatic mechanism of DNA methyltransferases is unusual, because these enzymes flip their target base out of the DNA helix and, thereby, locally disrupt the B-DNA helix. This review describes the biological functions of DNA methylation in bacteria, fungi, plants, and mammals. In addition, the structures and mechanisms of the DNA methyltransferases, which enable them to specifically recognize their DNA targets and to induce such large conformational changes of the DNA, are discussed.
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                Author and article information

                Contributors
                Yasuko Kobayashi: +81-27-2208205 , +81-221-821 , kobayasu@gunma-u.ac.jp
                Journal
                Journal ID (nlm-ta): Pediatr Nephrol
                Journal ID (iso-abbrev): Pediatr. Nephrol
                Title: Pediatric Nephrology (Berlin, Germany)
                Publisher: Springer-Verlag (Berlin/Heidelberg )
                ISSN (Print): 0931-041X
                ISSN (Electronic): 1432-198X
                Publication date (Electronic): 2 August 2012
                Publication date PMC-release: 2 August 2012
                Publication date (Print): December 2012
                Volume: 27
                Issue: 12
                Pages: 2233-2241
                Affiliations
                [1 ]Department of Pediatrics, Gunma University Graduate School of Medicine, 3-39-22 Showa-machi, Maebashi, Gunma 371-8511 Japan
                [2 ]Department of Pediatrics, Gunma Chuo General Hospital, Maebashi, Gunma Japan
                [3 ]Gunma Children’s Medical Center, Hokkitsumura, Seta-gun, Gunma Japan
                [4 ]Kitakanto Allergy Institute, Midorishi, Gunma Japan
                [5 ]Laboratory of Genome Science, Biosignal Genome Resource Center, Gunma University Institute for Molecular and Cellular Regulation, Maebashi, Gunma Japan
                Article
                Publisher ID: 2248
                DOI: 10.1007/s00467-012-2248-z
                PMC ID: 3491205
                PubMed ID: 22855301
                SO-VID: 7af39438-8513-45b9-a15f-1003c34472c0
                Copyright © © The Author(s) 2012
                History
                Date received : 5 January 2012
                Date revision received : 31 May 2012
                Date accepted : 11 June 2012
                Categories
                Subject: Original Article
                Custom metadata
                issue-copyright-statement © IPNA 2012

                ScienceOpen disciplines: Nephrology
                Keywords: dna methylation,nephrotic syndrome,monocytes,naive t helper cells,microarray-based integrated analysis of methylation by isoschizomers (miami) method,genome-wide,children
                Data availability:
                ScienceOpen disciplines: Nephrology
                Keywords: dna methylation, nephrotic syndrome, monocytes, naive t helper cells, microarray-based integrated analysis of methylation by isoschizomers (miami) method, genome-wide, children

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