Epigenetic changes in renal genes dysregulated in mouse and rat models of type 1 diabetes.
作者： Radko Komers , Daniel Mar , Oleg Denisenko , Bei Xu , Terry T Oyama
DOI: 10.1038/LABINVEST.2013.47
关键词: EZH2 、 Biology 、 Gene 、 Molecular biology 、 Methyltransferase 、 Histone H3 、 Chromatin 、 Epigenetics 、 Demethylase 、 Gene silencing
摘要: Epigenetic processes are increasingly being recognized as factors in the pathophysiology of diabetes complications, but few chromatin studies have been done diabetic nephropathy (DN). We hypothesized that changes mRNA expression DN-related genes associated with epigenetic alterations and aberrant histone-modifying enzymes. RT-PCR a matrix–chromatin immunoprecipitation platform were used to examine renal expression, RNA polymerase II (Pol II) recruitment, marks at mouse (OVE26) streptozotocin-induced rat models type 1 diabetes. Diabetes induced Cox2, S100A4/FSP-1, vimentin both DN. Mcp-1 laminin γ1 (Lamc1) increased mice not rats. Comparison Pol levels suggested diabetes-induced these transcripts is mediated by transcriptional posttranscriptional processes. Decreases histone H3 lysine 27 tri-methylation (H3K27m3, silencing mark) increases 4 di-methylation (H3K4m2, activating most consistent tested genes. In agreement results, immunoblot analysis showed protein abundance H3K27m2/3 demethylase KDM6A, no cognate methyltransferase Ezh2 kidneys OVE26 compared controls. rats, was higher without demonstrating mechanisms DN-induced H3K27m3 loss could be species specific. summary, we show altered some recruitment corresponding decrease repressive selected loci, least equivalent This pattern contribute diabetes-mediated transitions facilitate kidney.
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