RNA sequencing of mouse carotid arteries after sacubitril/valsartan treatment
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ABSTRACT:
PROVIDER: PRJNA532452 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Purpose: To get insight into mouse strain-dependent differences in vascular remodeling, we analyzed gene expression profiles of the ligated carotid arteries after interventions in C57BL/6J and 129X1/SvJ mice Methods: mRNA isolations from snap-frozen single carotids (n=3 per group) were conducted. Tissue homogenization by Next Advance Bullet Blender with zirconium oxide beads and Trizol. Total RNA isolation using Trizol and Qiagen RNeasy Micro kit. Results: Multiple quality controls showed a reliable RNAseq of mRNAs from the ligated carotid arteries. Specifically, there was less than 2.6% drop in reads that ranged between 26.5 to 37.7 million reads. We found a good alignment and mapping to a mouse genome (82.4 - 91.0%) in this RNAseq study. A differential gene expression analysis was done by DESeq2-1.16.1 within R-3.4.1 for data normalization and differential expression analysis with an adjusted p-value threshold of 0.05 on each set of raw expression measures. Conclusions: Our study shows significant differences in gene expression signatures in carotid arteries from two inbred mouse strains after sacubitril/valsartan treatment. We conclude that genetic background determines efficacy of the sacubitril/valsartan in mice.
2020-04-10 | GSE129689 | GEO
Project description:The whole rat genome microarray expression profiling of carotid artery specimen was emplyed to identify the gene expression profile before and after balloon injury. In our study, the neointimal formation of carotid arteries was apparent at day 7 and markedly increased at day 21 after balloon injury. In order to investigate the underlying mechanism of neointimal formationin in injured carotid arteries, all genes involved in signaling pathways whose expression was altered 2-fold in injured carotid arteries at day 7 and day 21 as compared to uninjured arteries were filtered out. Expression of four genes (TLR4, IRAK1, IκBα, IL-1β) from TLR signaling pathway was quantified in the same RNA samples by quantitative real-time PCR, conforming that TLR signaling pathway participated in neointimal formation of carotid arteries after balloon injury.
2013-06-29 | GSE48279 | GEO
Project description:The whole rat genome microarray expression profiling of carotid artery specimen was emplyed to identify the gene expression profile before and after balloon injury. In our study, the neointimal formation of carotid arteries was apparent at day 7 and markedly increased at day 21 after balloon injury. In order to investigate the underlying mechanism of neointimal formationin in injured carotid arteries, all genes involved in signaling pathways whose expression was altered 2-fold in injured carotid arteries at day 7 and day 21 as compared to uninjured arteries were filtered out. Expression of four genes (TLR4, IRAK1, IM-NM-:BM-NM-1, IL-1M-NM-2) from TLR signaling pathway was quantified in the same RNA samples by quantitative real-time PCR, conforming that TLR signaling pathway participated in neointimal formation of carotid arteries after balloon injury. Balloon injury-induced gene expression in wistar rat was measured at day 7 and day 21 after balloon injury as compared with uninjured arteries. Two independent experiments were performed at each time (uninjured, day 7 or day 21) using different wistar rats for each experiment.
2013-06-29 | E-GEOD-48279 | biostudies-arrayexpress
Project description:IRF9 is ubiquitously expressed and mediates the effects of IFNs, previous study showed that IRF9 played an important role in immunity and cell fate decision. Our recent study revealed that IRF9 involved in cardiac hypertrophy, hepatic steatosis and insulin resistance. However, the function of IRF9 in VSMC and neointima formation was largely unknown. We found that IRF9 expression was significantly increased in the VSMCs of mouse carotid artery. More importantly, we generated SMC-specific IRF9 overexpression transgenic mice (IRF9 TG) and found that IRF9 TG significantly increased VSMC proliferation, migration and neointima formation compared with NTG mice in response to injury. To evaluate the underlying mechanism by which IRF9 promotes VSMC proliferation and migration after vascular injury, IRF9 TG and NTG mice were subjected to wire-injury and the carotid arteries were collected at 14 days post-injury. We combined 3-5 vessels for one sample, and 3 samples for each phenotype. Subsequently, a total of 400ng RNA was used following Affymetrix instruction and 10 ug of cRNA were hybridized for 16 hr at 45°. GeneChips were scanned using the Scanner 7G and the data was analyzed with Expression Console using Affymetrix default analysis settings and global scaling as normalization method. RMA analysis was employed to evaluate the gene expression. We used microarrays to detect the global gene expression in the carotid arteries of smooth muscle cell specific IRF9 transgenic mice(IRF9 TG) compared with non transgenic control mice (NTG) at 14 days post-injury and identified distinct classes of altered genes.
2014-09-03 | GSE61046 | GEO
Project description:IRF4 is mainly expressed in immune cells, including B cell, T cell, macrophage and dendritic cell. Previous study showed that IRF4 plays important roles in regulating the differentiation and maturation of immune cells. Recently, our and other`s studies revealed that IRF4 involved in the pathogenesis of cardiac hypertrophy, cerebral ischemic reperfusion injury and metabolic disorder. However, the function of IRF4 in VSMC and neointima formation was largely unknown. We found that IRF4 expression was dramatically decreased in the VSMCs of mouse carotid artery. More importantly, using global IRF4 deficient mouse (KO), we demonstrated that IRF4 deficiency significantly increased VSMC proliferation, migration and neointima formation compared with wild type mice (WT) in response to injury. To evaluate the underlying mechanism by which IRF4 promotes VSMC proliferation and migration after vascular injury, IRF4 KO and WT mice were subjected to wire-injury and the carotid arteries were collected at 14 days post-injury. We combined 3-5 vessels for one sample, and 3 samples for each phenotype. Subsequently, a total of 400ng RNA was used following Affymetrix instruction and 10 ug of cRNA were hybridized for 16 hr at 45°. GeneChips were scanned using the Scanner 7G and the data was analyzed with Expression Console using Affymetrix default analysis settings and global scaling as normalization method. RMA analysis was employed to evaluate the gene expression. We used microarrays to detect the global gene expression in the carotid arteries of IRF4 knockout mice (IRF4 KO) compared with wild type mice (WT) at 14 days post-injury and identified distinct classes of altered genes
2019-10-15 | GSE88930 | GEO
Project description:IRF9 is ubiquitously expressed and mediates the effects of IFNs, previous study showed that IRF9 played an important role in immunity and cell fate decision. Our recent study revealed that IRF9 involved in cardiac hypertrophy, hepatic steatosis and insulin resistance. However, the function of IRF9 in VSMC and neointima formation was largely unknown. We found that IRF9 expression was significantly increased in the VSMCs of mouse carotid artery. More importantly, we generated SMC-specific IRF9 overexpression transgenic mice (IRF9 TG) and found that IRF9 TG significantly increased VSMC proliferation, migration and neointima formation compared with NTG mice in response to injury. To evaluate the underlying mechanism by which IRF9 promotes VSMC proliferation and migration after vascular injury, IRF9 TG and NTG mice were subjected to wire-injury and the carotid arteries were collected at 14 days post-injury. We combined 3-5 vessels for one sample, and 3 samples for each phenotype. Subsequently, a total of 400ng RNA was used following Affymetrix instruction and 10 ug of cRNA were hybridized for 16 hr at 45°. GeneChips were scanned using the Scanner 7G and the data was analyzed with Expression Console using Affymetrix default analysis settings and global scaling as normalization method. RMA analysis was employed to evaluate the gene expression. We used microarrays to detect the global gene expression in the carotid arteries of smooth muscle cell specific IRF9 transgenic mice(IRF9 TG) compared with non transgenic control mice (NTG) at 14 days post-injury and identified distinct classes of altered genes. non-transgenic controls mice (NTG) and smooth muscle specific IRF9 transgenic mice (IRF9 TG) were subjected to wire-injury and the carotid ateries were collected at 14 days post-injury. We combine 3-5 vessels in one tube and for a single Affymetrix microarray. Total RNA was extracted and a total of 400ng RNA was used following Affymetrix instruction. 3 biological samples for each genotype.
2014-09-03 | E-GEOD-61046 | biostudies-arrayexpress
Project description:Our objective is to identify new miRNAs and their target mRNAs involved in arterial stenosis, especially pathological changes of smooth muscle cells. To this end, the balloon injury model was used to induce the activation of smooth muscle cells by damaging arterial endothelial cells. The balloon-injured rat carotid arteries were isolated and subjected to the RNA-Seq. Note: Raw sequencing data have been lost for this dataset.
2022-10-01 | E-MTAB-11057 | biostudies-arrayexpress
Project description:Our objective is to identify new miRNAs and their target mRNAs involved in arterial stenosis, especially pathological changes of smooth muscle cells. To this end, the balloon injury model was used to induce the activation of smooth muscle cells by damaging arterial endothelial cells. The balloon-injured rat carotid arteries were isolated and subjected to the RNA-Seq.
2022-10-01 | E-MTAB-11100 | biostudies-arrayexpress
Project description:Single-cell RNA sequencing of the rat carotid arteries uncovers mechanisms of in-stent restenosis
| PRJNA728289 | ENA
Project description:Purpose: To determine the effect of disturbed blood flow and aging on mouse carotid artery endothelial cells. Methods: 8-week old and 80-week-old male C57BL6 mice were subjected to partial carotid ligation surgery and two days post ligation surgery, the endothelial enriched RNAs were flushed out using Qiazol
2024-02-07 | GSE197366 | GEO