Epigenetic and Transcriptional regulation of the Human Angiotensinogen Gene by High Salt
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ABSTRACT:
PROVIDER: PRJNA1018987 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26113700_1.fastq.gz | Fastqsanger.gz | |||
| SRR26113700_2.fastq.gz | Fastqsanger.gz | |||
| SRR26113701_1.fastq.gz | Fastqsanger.gz | |||
| SRR26113701_2.fastq.gz | Fastqsanger.gz | |||
| SRR26113702_1.fastq.gz | Fastqsanger.gz |
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Project description:Hypertension is caused by a combination of genetic and environmental factors. Angiotensinogen (AGT) is a component of RAAS, that regulates blood pressure. The human AGT (hAGT) gene has -6A/-6G polymorphism and -6A variant is associated with human hypertension. In this study, we have investigated the epigenetic regulation of the hAGT gene. To understand transcriptional regulation of the hAGT, we have made transgenic animals containing -6A. We show that HS affects DNA methylation and modulates transcriptional regulation of this gene in liver and kidney. HS increases hAGT gene expression in -6A TG mice. We have observed that the number of CpG sites in the hAGT promoter is decreased after HS treatment. In the liver, four CpG sites are methylated whereas after HS treatment, only two CpG sites observed. In the kidney, five CpG sites are methylated, whereas after HS treatment, only three CpG sites are observed. These results suggest that HS promotes DNA demethylation and increasing AGT gene expression. RT-PCR and immunoblot analysis show that hAGT gene expression is increased after HS treatment. Chip assay has shown that transcription factors bind strongly after HS treatment. RNA-Seq analysis identified differentially expressed genes, canonical pathways, upstream regulators. One of the plausible mechanisms for HS induced up-regulation of the hAGT gene is through IL-6/JAK/STAT3/AGT axis.
2023-12-13 | GSE243600 | GEO
Project description:Hypertension is caused by a combination of genetic and environmental factors. Angiotensinogen (AGT) is a component of RAAS, that regulates blood pressure. The human angiotensinogen (hAGT) gene has -6A/-6G polymorphism and -6A variant is associated with human hypertension. In this study, we have investigated the epigenetic regulation of the hAGT. To understand transcriptional regulation of the hAGT, we have made transgenic animals containing -6A. We show that HS affects DNA methylation and modulates transcriptional regulation of this gene in liver and kidney. High salt (HS) increases hAGT gene expression in -6A TG mice. We have observed that the number of CpG sites in the hAGT promoter is decreased after HS treatment. In the liver, seven CpG sites are methylated whereas after HS treatment, only three CpG sites remain methylated. In the kidney, five CpG sites are methylated, whereas after HS treatment, only three CpG sites remain methylated. These results suggest that HS promotes DNA demethylation and increasing AGT gene expression. RT-PCR and immunoblot analysis show that hAGT gene expression is increased by HS. Chip assay has shown that transcription factors bind strongly after HS treatment. RNA-Seq identified differentially expressed genes, novel target genes associated with hypertension, top canonical pathways, upstream regulators. One of the plausible mechanisms for HS induced up-regulation of the hAGT gene is through IL-6/JAK/STAT3/AGT axis.
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Project description:Investigation of differential gene regulation with overexpression of angiotensinogen in white adipose tissue. We hypothesized that angiotensinogen overexpression will disrupt metabolic homeostasis of adipocytes leading to obesity and related chronic diseases. Results indicate that angiotensinogen overexpression differentially regulate genes related metabolic functions in adipose tissue.
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Project description:Purpose: Our previous study has confirmed that reduction of SIRT3 expression is a main factor contributing to salt-induced hepatic inflammtion. Here we sought to investigate whether salt-induced SIRT3 reduction was related to epigenetic modification. Methods: 6-week-old male SIRT3 knockout or their wild-type littermates were fed with high salt diet (HSD, containing 8% NaCl) or normal salt diet (NSD, containing 0.4% NaCl) for 4 months. And then their liver tissues were removed and subjected to ChIP-seq using antibodies against H3K27ac (ab4729), H3K4me1 (ab8895), H3K9ac (39917) and H3 (ab1791). Results: Through ChIP-seq, we observed the enrichment of H3K27ac was increased on the promoters of Sirt3 and some pro-inflammatory genes, including Ccl2, Tnf and Il6, after high salt loading. However, neither H3K4me1 nor H3K9ac displayed such phenomunum. In addition, those genes containing increased H3K27ac level in response to high salt were mainly enriched in metabolism and inflammatory pathways. And knockout of SIRT3 mainly affected genes related to AMP-activated protein kinase (AMPK) and insulin signaling pathways. Conclusions: Salt-induced SIRT3 reduction is related to the epigenetic regulation, especially H3K27ac.
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Project description:Purpose: Our previous study has confirmed that reduction of SIRT3 expression is a main factor contributing to salt-induced hepatic inflammtion. Here we sought to investigate whether salt-induced SIRT3 reduction was related to epigenetic modification. Methods: 6-week-old male wild-type mice were fed with high salt diet (HSD, containing 8% NaCl) or normal salt diet (NSD, containing 0.4% NaCl) for 4 months. And then their liver tissues were removed and subjected to bilsulfate-seq. Results: Through bisulfate-seq, we did not observe any change in DNA methylation in the CpG island of Sirt3 gene promoter region. Conclusions: Salt-induced SIRT3 reduction is not related to DNA methylation on SIRT3 gene promoter.
2023-09-01 | GSE183583 | GEO
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Project description:We report the comparison of low salt vs high salt diet fed Dahl rat kidney glomeruli by sequencing analysis
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Project description:Genome wide gene expression analysis of mRNA siolated from whole heart tissue from wild type and cardiomyocyte selective MR null mice. The role of mineralocorticoid receptors (MR) in specific cell types of the myocardium in cardiac remodeling remains unknown. We investigated MR in cardiomyocytes in DOC/salt-induced cardiac pathology. Cardiomyocyte MR-null mice (CM-MRKO) and control mice (WT) were given DOC/salt and cardiac responses were examined at 8 days and 8 weeks. Cardiac function in untreated mice wild type and CM-MRKO mice was determined by Langendorf and showed no differences. At 8 days CM-MRKO showed equivalent monocyte/macrophage recruitment to wild type mice in response to DOC/salt treatment. Profibrotic markers were significantly reduced in CM-MRKO hearts at base line and in response to DOC/salt. In contrast, at 8 weeks CM-MRKO mice showed no DOC/salt-induced increase in inflammatory cell infiltrate, fibrosis or systolic blood pressure (SBP). Similarly, DOC/salt-mediated increases in proinflammatory and profibrotic gene expression were not detected in CM-MRKO mice. Although mRNA levels for fibronectin and collagen III were similar for each genotype, this was not translated into protein expression. Interestingly, untreated CM-MRKO mice showed increased mRNA and protein for decorin and a further increase with DOC/salt. Together, these data suggest a direct role for cardiomyocyte MR in DOC/salt-induced tissue remodelling and SBP regulation. Moreover, a specific profibrotic pathway is dysregulated in CM-MRKO mice, suggesting a potential mechanism for the cardioprotective effects of selective MR deletion in cardiomyocytes.
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