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Article ; Online: Fine tuning gene expression: the epigenome.

Mohtat, Davoud / Susztak, Katalin

2010 Volume 30, Issue 5, Page(s) 468–476

Abstract: An epigenetic trait is a stably inherited phenotype resulting from changes in a chromosome without alterations in the DNA sequence. Epigenetic modifications such as DNA methylation, together with covalent modification of histones, are thought to alter ... ...

Abstract	An epigenetic trait is a stably inherited phenotype resulting from changes in a chromosome without alterations in the DNA sequence. Epigenetic modifications such as DNA methylation, together with covalent modification of histones, are thought to alter chromatin density and accessibility of the DNA to cellular machinery, thereby modulating the transcriptional potential of the underlying DNA sequence. As environmental changes influence epigenetic marks, epigenetics provides an added layer of variation that might mediate the relationship between genotype and internal and external environmental factors. Integration of our knowledge in genetics, epigenomics, and genomics with the use of systems biology tools may present investigators with new, powerful tools to study many complex human diseases such as kidney disease.
MeSH term(s)	Animals ; Chronic Disease ; CpG Islands ; DNA Methylation ; Epigenesis, Genetic ; Epigenomics ; Gene Expression ; Histones/metabolism ; Humans ; Kidney Diseases/genetics ; Systems Biology
Chemical Substances	Histones
Language	English
Publishing date	2010-11-02
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	604652-6
ISSN	1558-4488 ; 0270-9295
ISSN (online)	1558-4488
ISSN	0270-9295
DOI	10.1016/j.semnephrol.2010.07.004
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Article ; Online: Urinary transforming growth factor beta-1 as a marker of renal dysfunction in sickle cell disease.

Mohtat, Davoud / Thomas, Rosemary / Du, Zangfang / Boakye, Yaa / Moulton, Thomas / Driscoll, Catherine / Woroniecki, Robert

Pediatric nephrology (Berlin, Germany)

2010 Volume 26, Issue 2, Page(s) 275–280

Abstract: Renal dysfunction affects 5-18% of patients with sickle cell disease (SCD). To date, no studies have described urinary levels of transforming growth factor β-1 (TGF-β1), a marker of fibrosis, and neutrophil gelatinase-associated lipocalin (NGAL), a ... ...

Abstract	Renal dysfunction affects 5-18% of patients with sickle cell disease (SCD). To date, no studies have described urinary levels of transforming growth factor β-1 (TGF-β1), a marker of fibrosis, and neutrophil gelatinase-associated lipocalin (NGAL), a marker of acute/chronic kidney disease, as biomarkers in identifying patients at risk of developing renal disease in SCD. We hypothesized that SCD subjects will have increased urinary excretion of TGF-β1 and NGAL compared with healthy controls (CTR). We examined 51 SCD subjects: 42 HbSS, 8 HbSC, and 1 HbSD. Sixteen out of 42 patients with HbSS were on hydroxyurea (HU). Urinary excretion of TGF-β1 was 26.4 ± 1.5 pg/mgCr in SCD subjects vs 15.0 ± 2.4 pg/mgCr in CTR (p<0.00001). SCD patients with hemoglobin < 9 g/dl had higher urinary TGF-β1 than patients with milder anemia (p=0.002). Urinary TGF-β1 trended lower in HbSS patients treated with HU (23.61 ± 2.6 pg/mgCr), vs patients not on HU (27.69 ± 1.8 pg/mgCr; p=0.055). There was no correlation between urinary TGF-β1 and microalbuminuria or estimated glomerular function. There was no difference in urinary NGAL in SCD patients vs CTR. We suggest that urinary TGF-β1 may serve as a marker of early renal injury in SCD.
MeSH term(s)	Acute-Phase Proteins/urine ; Adolescent ; Age Factors ; Albuminuria/metabolism ; Anemia, Sickle Cell/complications ; Biomarkers/urine ; Child ; Child, Preschool ; Female ; Glomerular Filtration Rate ; Humans ; Kidney Diseases/diagnosis ; Kidney Diseases/etiology ; Kidney Diseases/urine ; Lipocalin-2 ; Lipocalins/urine ; Male ; Proto-Oncogene Proteins/urine ; Transforming Growth Factor beta/urine ; Young Adult
Chemical Substances	Acute-Phase Proteins ; Biomarkers ; LCN2 protein, human ; Lipocalin-2 ; Lipocalins ; Proto-Oncogene Proteins ; Transforming Growth Factor beta
Language	English
Publishing date	2010-11-25
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	631932-4
ISSN	1432-198X ; 0931-041X
ISSN (online)	1432-198X
ISSN	0931-041X
DOI	10.1007/s00467-010-1677-9
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Article ; Online: Transcriptome analysis of human diabetic kidney disease.

Woroniecka, Karolina I / Park, Ae Seo Deok / Mohtat, Davoud / Thomas, David B / Pullman, James M / Susztak, Katalin

Diabetes

2011 Volume 60, Issue 9, Page(s) 2354–2369

Abstract: Objective: Diabetic kidney disease (DKD) is the single leading cause of kidney failure in the U.S., for which a cure has not yet been found. The aim of our study was to provide an unbiased catalog of gene-expression changes in human diabetic kidney ... ...

Abstract	Objective: Diabetic kidney disease (DKD) is the single leading cause of kidney failure in the U.S., for which a cure has not yet been found. The aim of our study was to provide an unbiased catalog of gene-expression changes in human diabetic kidney biopsy samples. Research design and methods: Affymetrix expression arrays were used to identify differentially regulated transcripts in 44 microdissected human kidney samples. DKD samples were significant for their racial diversity and decreased glomerular filtration rate (~25-35 mL/min). Stringent statistical analysis, using the Benjamini-Hochberg corrected two-tailed t test, was used to identify differentially expressed transcripts in control and diseased glomeruli and tubuli. Two different web-based algorithms were used to define differentially regulated pathways. Results: We identified 1,700 differentially expressed probesets in DKD glomeruli and 1,831 in diabetic tubuli, and 330 probesets were commonly differentially expressed in both compartments. Pathway analysis highlighted the regulation of Ras homolog gene family member A, Cdc42, integrin, integrin-linked kinase, and vascular endothelial growth factor signaling in DKD glomeruli. The tubulointerstitial compartment showed strong enrichment for inflammation-related pathways. The canonical complement signaling pathway was determined to be statistically differentially regulated in both DKD glomeruli and tubuli and was associated with increased glomerulosclerosis even in a different set of DKD samples. Conclusions: Our studies have cataloged gene-expression regulation and identified multiple novel genes and pathways that may play a role in the pathogenesis of DKD or could serve as biomarkers.
MeSH term(s)	Adult ; Aged ; Cross-Sectional Studies ; Diabetic Nephropathies/genetics ; Diabetic Nephropathies/metabolism ; Diabetic Nephropathies/pathology ; Female ; Gene Expression Profiling ; Gene Expression Regulation ; Humans ; Kidney Glomerulus/metabolism ; Kidney Glomerulus/pathology ; Male ; Middle Aged
Language	English
Publishing date	2011-07-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80085-5
ISSN	1939-327X ; 0012-1797
ISSN (online)	1939-327X
ISSN	0012-1797
DOI	10.2337/db10-1181
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Article ; Online: Cytosine methylation changes in enhancer regions of core pro-fibrotic genes characterize kidney fibrosis development.

Ko, Yi-An / Mohtat, Davoud / Suzuki, Masako / Park, Ae Seo Deok / Izquierdo, Maria Concepcion / Han, Sang Youb / Kang, Hyun Mi / Si, Han / Hostetter, Thomas / Pullman, James M / Fazzari, Melissa / Verma, Amit / Zheng, Deyou / Greally, John M / Susztak, Katalin

Genome biology

2013 Volume 14, Issue 10, Page(s) R108

Abstract: Background: One in eleven people is affected by chronic kidney disease, a condition characterized by kidney fibrosis and progressive loss of kidney function. Epidemiological studies indicate that adverse intrauterine and postnatal environments have a ... ...

Abstract	Background: One in eleven people is affected by chronic kidney disease, a condition characterized by kidney fibrosis and progressive loss of kidney function. Epidemiological studies indicate that adverse intrauterine and postnatal environments have a long-lasting role in chronic kidney disease development. Epigenetic information represents a plausible carrier for mediating this programming effect. Here we demonstrate that genome-wide cytosine methylation patterns of healthy and chronic kidney disease tubule samples obtained from patients show significant differences. Results: We identify differentially methylated regions and validate these in a large replication dataset. The differentially methylated regions are rarely observed on promoters, but mostly overlap with putative enhancer regions, and they are enriched in consensus binding sequences for important renal transcription factors. This indicates their importance in gene expression regulation. A core set of genes that are known to be related to kidney fibrosis, including genes encoding collagens, show cytosine methylation changes correlating with downstream transcript levels. Conclusions: Our report raises the possibility that epigenetic dysregulation plays a role in chronic kidney disease development via influencing core pro-fibrotic pathways and can aid the development of novel biomarkers and future therapeutics.
MeSH term(s)	Aged ; Base Sequence ; Binding Sites ; Case-Control Studies ; Cluster Analysis ; Cytosine/metabolism ; DNA Methylation ; Enhancer Elements, Genetic ; Fibrosis ; Gene Expression Profiling ; Gene Expression Regulation/drug effects ; Gene Regulatory Networks ; Humans ; Kidney/metabolism ; Kidney/pathology ; Middle Aged ; Nucleotide Motifs ; Position-Specific Scoring Matrices ; Renal Insufficiency, Chronic/genetics ; Renal Insufficiency, Chronic/pathology ; Reproducibility of Results ; Transcription Factors ; Transcription, Genetic/drug effects
Chemical Substances	Transcription Factors ; Cytosine (8J337D1HZY)
Language	English
Publishing date	2013-10-08
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2040529-7
ISSN	1474-760X ; 1474-760X
ISSN (online)	1474-760X
ISSN	1474-760X
DOI	10.1186/gb-2013-14-10-r108
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Article: Cytosine methylation changes in enhancer regions of core pro-fibrotic genes characterize kidney fibrosis development

Genome biology. 2013 Oct., v. 14, no. 10

2013

Abstract: BACKGROUND: One in eleven people is affected by chronic kidney disease, a condition characterized by kidney fibrosis and progressive loss of kidney function. Epidemiological studies indicate that adverse intrauterine and postnatal environments have a ... ...

Abstract	BACKGROUND: One in eleven people is affected by chronic kidney disease, a condition characterized by kidney fibrosis and progressive loss of kidney function. Epidemiological studies indicate that adverse intrauterine and postnatal environments have a long-lasting role in chronic kidney disease development. Epigenetic information represents a plausible carrier for mediating this programming effect. Here we demonstrate that genome-wide cytosine methylation patterns of healthy and chronic kidney disease tubule samples obtained from patients show significant differences. RESULTS: We identify differentially methylated regions and validate these in a large replication dataset. The differentially methylated regions are rarely observed on promoters, but mostly overlap with putative enhancer regions, and they are enriched in consensus binding sequences for important renal transcription factors. This indicates their importance in gene expression regulation. A core set of genes that are known to be related to kidney fibrosis, including genes encoding collagens, show cytosine methylation changes correlating with downstream transcript levels. CONCLUSIONS: Our report raises the possibility that epigenetic dysregulation plays a role in chronic kidney disease development via influencing core pro-fibrotic pathways and can aid the development of novel biomarkers and future therapeutics.
Keywords	DNA methylation ; biomarkers ; data collection ; epidemiological studies ; epigenetics ; fibrosis ; gene expression regulation ; genes ; kidneys ; patients ; renal function ; therapeutics ; transcription factors
Language	English
Dates of publication	2013-10
Size	p. 3159.
Publishing place	Springer-Verlag
Document type	Article
ZDB-ID	2040529-7
ISSN	1474-760X ; 1465-6914 ; 1465-6906
ISSN (online)	1474-760X ; 1465-6914
ISSN	1465-6906
DOI	10.1186/gb-2013-14-10-r108
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Kidney cancer is characterized by aberrant methylation of tissue-specific enhancers that are prognostic for overall survival.

Hu, Caroline Y / Mohtat, Davoud / Yu, Yiting / Ko, Yi-An / Shenoy, Niraj / Bhattacharya, Sanchari / Izquierdo, Maria C / Park, Ae Seo Deok / Giricz, Orsolya / Vallumsetla, Nishanth / Gundabolu, Krishna / Ware, Kristin / Bhagat, Tushar D / Suzuki, Masako / Pullman, James / Liu, X Shirley / Greally, John M / Susztak, Katalin / Verma, Amit

Clinical cancer research : an official journal of the American Association for Cancer Research

2014 Volume 20, Issue 16, Page(s) 4349–4360

Abstract: Purpose: Even though recent studies have shown that genetic changes at enhancers can influence carcinogenesis, most methylomic studies have focused on changes at promoters. We used renal cell carcinoma (RCC), an incurable malignancy associated with ... ...

Abstract	Purpose: Even though recent studies have shown that genetic changes at enhancers can influence carcinogenesis, most methylomic studies have focused on changes at promoters. We used renal cell carcinoma (RCC), an incurable malignancy associated with mutations in epigenetic regulators, as a model to study genome-wide patterns of DNA methylation at a high resolution. Experimental design: Analysis of cytosine methylation status of 1.3 million CpGs was determined by the HELP assay in RCC and healthy microdissected renal tubular controls. Results: We observed that the RCC samples were characterized by widespread hypermethylation that preferentially affected gene bodies. Aberrant methylation was particularly enriched in kidney-specific enhancer regions associated with H3K4Me1 marks. Various important underexpressed genes, such as SMAD6, were associated with aberrantly methylated, intronic enhancers, and these changes were validated in an independent cohort. MOTIF analysis of aberrantly hypermethylated regions revealed enrichment for binding sites of AP2a, AHR, HAIRY, ARNT, and HIF1 transcription factors, reflecting contributions of dysregulated hypoxia signaling pathways in RCC. The functional importance of this aberrant hypermethylation was demonstrated by selective sensitivity of RCC cells to low levels of decitabine. Most importantly, methylation of enhancers was predictive of adverse prognosis in 405 cases of RCC in multivariate analysis. In addition, parallel copy-number analysis from MspI representations demonstrated novel copy-number variations that were validated in an independent cohort of patients. Conclusions: Our study is the first high-resolution methylome analysis of RCC, demonstrates that many kidney-specific enhancers are targeted by aberrant hypermethylation, and reveals the prognostic importance of these epigenetic changes in an independent cohort.
MeSH term(s)	Biomarkers, Tumor/genetics ; Carcinoma, Renal Cell/genetics ; Carcinoma, Renal Cell/mortality ; Case-Control Studies ; Cells, Cultured ; Cohort Studies ; DNA Methylation ; Enhancer Elements, Genetic/genetics ; Epigenesis, Genetic/genetics ; Gene Expression Regulation, Neoplastic ; Humans ; Kidney Neoplasms/genetics ; Kidney Neoplasms/mortality ; Organ Specificity ; Prognosis ; Promoter Regions, Genetic ; RNA, Messenger/genetics ; Real-Time Polymerase Chain Reaction ; Reverse Transcriptase Polymerase Chain Reaction ; Survival Rate
Chemical Substances	Biomarkers, Tumor ; RNA, Messenger
Language	English
Publishing date	2014-06-10
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-14-0494
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Article: Cytosine methylation changes in enhancer regions of core pro-fibrotic genes characterize kidney fibrosis development

Genome biology

Volume v. 14,, Issue no. 1

Abstract	BACKGROUND: One in eleven people is affected by chronic kidney disease, a condition characterized by kidney fibrosis and progressive loss of kidney function. Epidemiological studies indicate that adverse intrauterine and postnatal environments have a long-lasting role in chronic kidney disease development. Epigenetic information represents a plausible carrier for mediating this programming effect. Here we demonstrate that genome-wide cytosine methylation patterns of healthy and chronic kidney disease tubule samples obtained from patients show significant differences. RESULTS: We identify differentially methylated regions and validate these in a large replication dataset. The differentially methylated regions are rarely observed on promoters, but mostly overlap with putative enhancer regions, and they are enriched in consensus binding sequences for important renal transcription factors. This indicates their importance in gene expression regulation. A core set of genes that are known to be related to kidney fibrosis, including genes encoding collagens, show cytosine methylation changes correlating with downstream transcript levels. CONCLUSIONS: Our report raises the possibility that epigenetic dysregulation plays a role in chronic kidney disease development via influencing core pro-fibrotic pathways and can aid the development of novel biomarkers and future therapeutics.
Keywords	data collection ; therapeutics ; genes ; renal function ; transcription factors ; biomarkers ; gene expression regulation ; kidneys ; patients ; epigenetics ; DNA methylation ; epidemiological studies ; fibrosis
Language	English
Document type	Article
ISSN	1465-6906
Database	AGRIS - International Information System for the Agricultural Sciences and Technology

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Article ; Online: Fine tuning gene expression: the epigenome.

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Article ; Online: Urinary transforming growth factor beta-1 as a marker of renal dysfunction in sickle cell disease.

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Article ; Online: Transcriptome analysis of human diabetic kidney disease.

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Article ; Online: Cytosine methylation changes in enhancer regions of core pro-fibrotic genes characterize kidney fibrosis development.

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Article: Cytosine methylation changes in enhancer regions of core pro-fibrotic genes characterize kidney fibrosis development

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Article ; Online: Kidney cancer is characterized by aberrant methylation of tissue-specific enhancers that are prognostic for overall survival.

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Article: Cytosine methylation changes in enhancer regions of core pro-fibrotic genes characterize kidney fibrosis development

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