RNA-seq Renin cells isolated from Ren1c-YFP mice with aortic coarctation
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE157699 | GEO | 2021/05/26
REPOSITORIES: GEO
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Project description:RNA-seq Renin cells isolated from Ren1c-YFP mice with aortic coarctation
| PRJNA662486 | ENA
Project description:RNA-seq was performed to compare the transcriptome of three renin cell types: juxtaglomerular cells, cells isolated from chronically recruited mice and in As4.1 cells
2020-10-31 | GSE117723 | GEO
Project description:The long term objective is to create an encyclopedia of the expression levels of all genes in multiple components of the developing kidney. The central thesis is straightforward. The combination of fluorescent activated cell sorting (FACS) plus microarray analysis offers a powerful, efficient and effective method for the creation of a global gene expression atlas of the developing kidney. Microarrays with essentially complete genome coverage can be used to quantitate expression levels of every gene in FACS isolated components of the developing kidney. The ensuing rapid read-out provides an expression atlas that is more sensitive, more economical and more complete than would be possible by in situ hybridizations alone. Renin-YFP transgenic mice were utilized to isolate renin producing cells from the kidneys of Adult mice treated with captopril, which was provided in the drinking water at a concentration of 0.5mg/ml. In addition, mice were given low-salt chow. Mice were treated for two weeks before renin producing cells were isolated from the kidney by fluorescent activated cell sorting (FACS). RNA was isolated from FACS sorted cells and the gene expression profiles were determined by microarrays.
2012-12-05 | E-GEOD-42712 | biostudies-arrayexpress
Project description:Chronic inflammation is known to contribute to the development of hypertension, but while the role of lymphocytes is well-established, the myeloid lineage, particularly as a possible mediator of renin-mediated hypertension, has not been studied. Vitamin D deficiency has pro-inflammatory consequences in monocytes, and it is linked to renin-mediated hypertension in mice. This prompted us to test the hypothesis that conditional knockout of the vitamin D receptor (VDR) in macrophages (KODMAC) would promote renin-dependent hypertension. We found that lack of macrophage vdr signaling was sufficient to induce high blood pressure (BP) in mice. Recipients of bone marrow from KODMAC mice experienced increased BP via activation of the renal renin-angiotensin system. Conversely BM transplants from mice with intact vdr signaling reduced BP in KODMAC mice by decreasing plasma renin and increasing urinary Na excretion. Deletion of myeloid vdr promotes vascular macrophage infiltration, increasing ROS-mediated scavenging of NO and reducing renal perfusion, resulting in increased plasma renin. Interestingly, deletion of macrophage vdr promotes their infiltration into the JG cell apparatus, regulating JG cell renin production by an unexpected communication between macrophages and JG cells through miR-106b-5p. Induction of macrophage endoplasmic reticulum stress phospho-PERK and CHOP pathways increased miR-106b-5p secretion, the uptake of which into JG cells induced renin production and release by repression of E2f1 and Pde3b transcription factors, constituting a novel mechanism by which inflammation causes hypertension.
2020-07-06 | GSE117704 | GEO
Project description:Local renin antiotensin systems have been identified for many extra-renal sites. Bone marrow has been proposed as one such site, although the nature of the renin-expressing cell type(s) has not been established. Affymetrix microarrays were used to characterize the expression profile of renin-expressing GFP positive cells.
2014-02-17 | GSE53916 | GEO
Project description:Background: Renin-expressing cells are myoendocrine cells crucial for survival which detect changes in blood pressure and release renin to maintain homeostasis. Renin is regulated through several pathways including cAMP, p300/CBP, and BET proteins including Brd4. Binding to the cAMP-responsive element in the renin enhancer region amplifies renin transcription and relies on each of these factors for an appropriate response. The specific regulatory changes that occur following inhibition of these pathways remains understudied. Therefore, we aimed to evaluate chromatin changes and gene signatures that occur following inhibition of renin regulatory factors. Methods: We treated As4.1 cells (a tumoral cell line that constitutively expresses renin) with three inhibitors (H89: PKA inhibition; JQ1: Brd4 inhibition; A-485: p300/CBP inhibition) that target required factors for renin transcriptional regulation. We then performed ATAC-seq, scRNA-seq, and ChIP-seq for H3K27ac and P300 binding on biological replicates of treated and control As4.1 cells. Results: Ren1 expression is significantly, but transiently, reduced following each inhibitory treatment. Further, PKA inhibition leads to corresponding losses in H3K27ac and p300 binding at the locus. A restricted set of nine genes with overlapping dynamically accessible regions, differential gene expression, and H3K27ac and p300 binding were identified with roles across three primary renin regulatory paradigms. Conclusions: The data shows that renin expression is regulated through a switch from an active to poised state of epigenetic control, a shift toward a less differentiated cellular identity via the loss of enhancer elements, and the disruption of cAMP, baroreceptor, and Notch mediated renin regulatory pathways.
2024-08-26 | GSE254943 | GEO
Project description:Background: Renin-expressing cells are myoendocrine cells crucial for survival which detect changes in blood pressure and release renin to maintain homeostasis. Renin is regulated through several pathways including cAMP, p300/CBP, and BET proteins including Brd4. Binding to the cAMP-responsive element in the renin enhancer region amplifies renin transcription and relies on each of these factors for an appropriate response. The specific regulatory changes that occur following inhibition of these pathways remains understudied. Therefore, we aimed to evaluate chromatin changes and gene signatures that occur following inhibition of renin regulatory factors. Methods: We treated As4.1 cells (a tumoral cell line that constitutively expresses renin) with three inhibitors (H89: PKA inhibition; JQ1: Brd4 inhibition; A-485: p300/CBP inhibition) that target required factors for renin transcriptional regulation. We then performed ATAC-seq, scRNA-seq, and ChIP-seq for H3K27ac and P300 binding on biological replicates of treated and control As4.1 cells. Results: Ren1 expression is significantly, but transiently, reduced following each inhibitory treatment. Further, PKA inhibition leads to corresponding losses in H3K27ac and p300 binding at the locus. A restricted set of nine genes with overlapping dynamically accessible regions, differential gene expression, and H3K27ac and p300 binding were identified with roles across three primary renin regulatory paradigms. Conclusions: The data shows that renin expression is regulated through a switch from an active to poised state of epigenetic control, a shift toward a less differentiated cellular identity via the loss of enhancer elements, and the disruption of cAMP, baroreceptor, and Notch mediated renin regulatory pathways.
2024-08-26 | GSE254944 | GEO
Project description:Background: Renin-expressing cells are myoendocrine cells crucial for survival which detect changes in blood pressure and release renin to maintain homeostasis. Renin is regulated through several pathways including cAMP, p300/CBP, and BET proteins including Brd4. Binding to the cAMP-responsive element in the renin enhancer region amplifies renin transcription and relies on each of these factors for an appropriate response. The specific regulatory changes that occur following inhibition of these pathways remains understudied. Therefore, we aimed to evaluate chromatin changes and gene signatures that occur following inhibition of renin regulatory factors. Methods: We treated As4.1 cells (a tumoral cell line that constitutively expresses renin) with three inhibitors (H89: PKA inhibition; JQ1: Brd4 inhibition; A-485: p300/CBP inhibition) that target required factors for renin transcriptional regulation. We then performed ATAC-seq, scRNA-seq, and ChIP-seq for H3K27ac and P300 binding on biological replicates of treated and control As4.1 cells. Results: Ren1 expression is significantly, but transiently, reduced following each inhibitory treatment. Further, PKA inhibition leads to corresponding losses in H3K27ac and p300 binding at the locus. A restricted set of nine genes with overlapping dynamically accessible regions, differential gene expression, and H3K27ac and p300 binding were identified with roles across three primary renin regulatory paradigms. Conclusions: The data shows that renin expression is regulated through a switch from an active to poised state of epigenetic control, a shift toward a less differentiated cellular identity via the loss of enhancer elements, and the disruption of cAMP, baroreceptor, and Notch mediated renin regulatory pathways.
2024-08-26 | GSE254941 | GEO
Project description:Background: Renin-expressing cells are myoendocrine cells crucial for survival which detect changes in blood pressure and release renin to maintain homeostasis. Renin is regulated through several pathways including cAMP, p300/CBP, and BET proteins including Brd4. Binding to the cAMP-responsive element in the renin enhancer region amplifies renin transcription and relies on each of these factors for an appropriate response. The specific regulatory changes that occur following inhibition of these pathways remains understudied. Therefore, we aimed to evaluate chromatin changes and gene signatures that occur following inhibition of renin regulatory factors. Methods: We treated As4.1 cells (a tumoral cell line that constitutively expresses renin) with three inhibitors (H89: PKA inhibition; JQ1: Brd4 inhibition; A-485: p300/CBP inhibition) that target required factors for renin transcriptional regulation. We then performed ATAC-seq, scRNA-seq, and ChIP-seq for H3K27ac and P300 binding on biological replicates of treated and control As4.1 cells. Results: Ren1 expression is significantly, but transiently, reduced following each inhibitory treatment. Further, PKA inhibition leads to corresponding losses in H3K27ac and p300 binding at the locus. A restricted set of nine genes with overlapping dynamically accessible regions, differential gene expression, and H3K27ac and p300 binding were identified with roles across three primary renin regulatory paradigms. Conclusions: The data shows that renin expression is regulated through a switch from an active to poised state of epigenetic control, a shift toward a less differentiated cellular identity via the loss of enhancer elements, and the disruption of cAMP, baroreceptor, and Notch mediated renin regulatory pathways.
2024-08-26 | GSE254940 | GEO
Project description:Regulated endocrine specific protein 18 (Resp18), expression has been specifically located in a series of tissues and cell types however the exact cellular function is unknown. In previous studies we have showed that a targeted disruption of Resp18 in Dahl SS rats (Resp18mutant) resulted in higher blood pressure (BP), increased renal fibrosis, and decreased survival rate on a long term (6-week) 2% high salt (HS) diet treatment compared with wild type SS rats. In the current study we studied whether a short term (1 week) exposure to HS diet shows a similar effect in Resp18mutant rats. Furthermore, previously we have shown that in addition to BP phenotype Resp18mutant rats have demonstrated deteriorative kidney phenotype evident through renal fibrosis, protein urea and protein cast formation. Based on this background we conducted BP study and performed transcriptomic profiling of the kidney after one-week exposure to HS diet treatment. Through radio-telemetry procedure, we found that the systolic BP was increased in the Resp18mutant rats compared with SS rats even with short term HS diet exposure. Therefore, we sought out to investigate if there was any alteration in the transcriptomic response by HS diet treatment in the Resp18mutant rat kidneys. Using RNA sequencing approach, we found that Resp18mutant rats showed a differential expression of 25 genes of which one was an upregulation of Ren. We confirmed the upregulation of Ren and other differentially expressed genes via qRT-PCR analysis. Upon KEGG pathway enrichment we found that the Resp18mutant rat showed upregulation in the renin angiotensin system (RAAS), and renin secretion pathway. Furthermore, the renin activity is found to be higher in Resp18mutant rats serum compared with SS rats. Therefore, these observations demonstrate that upon disruption of Resp18 gene in SS rats associated with the increase in renin secretion and thus increase BP.
2021-07-01 | GSE149006 | GEO