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 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:RNA-seq Renin cells isolated from Ren1c-YFP mice with aortic coarctation
| PRJNA662486 | ENA
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: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
Project description:Physical proximity mapping through sequencing can provide an unbiased view of the chromatin close to the proximal promoter of the renin gene (Ren). Our objective was to determine genomic regions that physically interact with the renin proximal promoter, using two different genetic backgrounds, the Dahl salt sensitive and normotensive SS-13BN, which have been shown to have different regulation of plasma renin in vivo. The chromatin conformation capture method with sequencing focused at the Ren proximal promoter in rat-derived cardiac endothelial cells was used. Cells were fixed, chromatin close to the Ren promoter was captured, and fragments were sequenced. The clustering of mapped reads produced a genome-wide map of chromatin in contact with the Ren promoter. The largest number of contacts was found on chromosome 13, the chromosome with Ren, and contacts were found on all other chromosomes except chromosome X. These contacts were significantly enriched with genes positively correlated with Ren expression and with mapped quantitative trait loci (QTLs) associated with blood pressure, cardiovascular and renal phenotypes. The results were reproducible in an independent biological replicate and in endothelial cells derived from a second rat stain. The findings reported here represent the first map between a critical cardiovascular gene and physical interacting loci throughout the genome, and will provide the basis for several new directions of research.
2019-02-14 | GSE110652 | GEO
Project description:This experiment was performed to study the expression profile of renin cells from mice subjected to homeostatic threat (hypotension). It was also used to compare expression of proliferation associated genes and tumor suppressors with existing cell line data.
2020-03-05 | GSE146386 | 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. Green fluorescent protein positive cells were sorted from whole bone marrow collected from adult transgenic mice. Bone marrow from several mice was collected and pooled on the day of a FACS sort. A portion of this was reserved for RNA extraction while the remainder was sorted. RNA was prepared with Trizol. Bone marrow collection and sorting was performed 3 times so that microarrays could be run in triplicate.
2014-02-17 | E-GEOD-53916 | biostudies-arrayexpress
Project description:High blood pressure is one of the major public health problems which causes severe disorders in several tissues including the human kidney. One of the most important signaling pathways associated with the regulation of blood pressure is the renin-angiotensin system (RAS), with its main mediator angiotensin II (ANGII). Elevated levels of circulating and intracellular ANGII and aldosterone lead to pro-fibrotic, -inflammatory and -hypertrophic milieu that causes remodelling and dysfunction in cardiovascular and renal tissues. Furthermore, ANGII has been recognized as major risk factor for the induction of apoptosis in podocytes, ultimately leading to chronic kidney disease (CKD). In the past, disease modeling of kidney-associated malignancies was extremely difficult, as the derivation of kidney originated cells is very challenging. Here we describe a differentiation protocol for reproducible differentiation of SIX2-positive urine derived renal progenitor cells (UdRPCs) into mature podocytes bearing typical foot processes. The UdRPCs-derived podocytes show the ability to execute Albumin endocytosis and the activation of the renin-angiotensin system by being responsive to ANGII stimulation. Our data reveals the ANGII dependent downregulation of NPHS1 and SYNPO, resulting in the disruption of the complex podocyte cytoskeletal architecture, as shown by immunofluorescence-based detection of α–ACTININ. In the present manuscript we confirm and propose UdRPCs as a unique cell type useful for studying nephrogenesis and associated diseases. Furthermore, the responsiveness of UdRPCs-derived podocytes to ANGII implies potential applications in nephrotoxicity studies and drug screening.
2022-03-31 | GSE171240 | GEO