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Genome‐wide analysis of histone H 3 lysine9 trimethylation by ChIP ‐seq in peripheral blood mononuclear cells of uremia patients
Author(s) -
Sui Weiguo,
He Huiyan,
Yan Qiang,
Chen Jiejing,
Zhang Ruohan,
Dai Yong
Publication year - 2013
Publication title -
hemodialysis international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.658
H-Index - 47
eISSN - 1542-4758
pISSN - 1492-7535
DOI - 10.1111/hdi.12051
Subject(s) - uremia , medicine , endocrinology
Treatment of uremia is now dominated by dialysis, in some cases, patients are treated with dialysis for decades, but overall outcomes are disappointing. A number of studies have confirmed the relevance of several experimental insights to the pathogenesis of uremia, but the specific biomarkers of uremia have not been fully elucidated. Studies of the epigenome have attracted little interest in nephrology, especially in uremia. However, to date, our knowledge about the alterations in histone methylation in uremia is unclear. H 3 K 9me3 variations were analyzed in peripheral blood mononuclear cells from 10 uremia patients and 10 healthy subjects, using chromatin immunoprecipitation followed by high‐throughput sequencing ( ChIP ‐seq). There were 96 genes with significantly different expressions in the uremia patients compared with the normal controls. Forty‐two increased and 54 decreased H 3 K 9me3 genes displaying significant differences were found in uremia patients compared with healthy subjects. Five positive genes, ras‐related C 3 botulinum toxin substrate 3 ( RAC 3), polycomb group ring finger 2 ( PCGF 2), myosin heavy chain 3 ( MYH 3), noggin ( NOG ), serpin peptidase inhibitor 8 ( SERPINB 8), were selected and quantified. Our studies indicate that there are significant alterations of H 3 K 9me3 in uremia patients; these significant H 3 K 9me3 candidates may help to explain the immunological disturbance and high cardiovascular complications in uremia patients. Such novel findings show the significance of H 3 K 9me3 as a potential biomarker or promising target for epigenetic‐based uremia therapies.