Mus musculus
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ABSTRACT:
PROVIDER: PRJNA260155 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Expression data from IRF4 KO mouse carotid arteries in response to wire-injury
| PRJNA349133 | ENA
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: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:We tried to identify mRNA targets of miR-126 involved in neointima formation in mice with an atherogenic background. Genome-wide expression profiling was carried out in wire-injured carotid arteries of miR-126+/+/ApoE-/- (control group) and miR-126-/-/ApoE-/- (target group) mice on western-type diet. RNA was isolated after 14 days following vascular injury (n=4 each group). Agilent SurePrint G3 Mouse GE Microarrays (8x60K format) were used in combination with a one-color based hybridization protocol. Signals on the microarrays were detected using the Agilent DNA Microarray Scanner. Differential gene expression was identified by applying appropriate biostatistics to the data set. GeneSpring GX11 analysis software was used to normalize and analyze the raw data Genomewide expression profile of miR-126+/+/ApoE-/- and miR-126-/-/ApoE-/- mice were measured at 14 days after vascular injury . 4 animals per group were used.
2014-02-19 | E-GEOD-34262 | 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: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:We tried to identify mRNA targets of miR-126 involved in neointima formation in mice with an atherogenic background. Genome-wide expression profiling was carried out in wire-injured carotid arteries of miR-126+/+/ApoE-/- (control group) and miR-126-/-/ApoE-/- (target group) mice on western-type diet. RNA was isolated after 14 days following vascular injury (n=4 each group). Agilent SurePrint G3 Mouse GE Microarrays (8x60K format) were used in combination with a one-color based hybridization protocol. Signals on the microarrays were detected using the Agilent DNA Microarray Scanner. Differential gene expression was identified by applying appropriate biostatistics to the data set. GeneSpring GX11 analysis software was used to normalize and analyze the raw data
2014-02-19 | GSE34262 | GEO
Project description:In order to identify microRNAs involved in neointima formation in mice with an atherogenic background, wire-induced carotid injury was performed in ApoE-/- mice on western-type diet. Uninjured carotid arteries served as control. RNA was isolated after 1, 7, 14, and 28 days (n=3-4 each group) and hybridized to an Agilent microRNA microarray (Sanger v12). Significantly regulated microRNAs (>2-fold) over time (P<0.05; ANOVA and Benjamini-Hochberg correction) were clustered by K-means algorithm. Distinct groups of similarly regulated microRNAs were detected in the course of neointima formation in hyperlipidemic mice.
2014-11-28 | GSE34054 | 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:To determine the differential expression of genes at sites of vascular injury in mice Four male, 5-6 mo old SMA-GFP mice (numbered 57, 60, 61, and 63) were subjected to fine wire femoral artery injury. The left femoral artery of each mouse was injured, and the contralateral artery was used as an uninjured control. The mice recovered from the injury procedure for 14 days, at which time they were sacrificed. The femoral arteries were removed and the adventitial side was extensively cleaned. The arteries were carefully opened longitudinally and immediately imaged for GFP. GFP-negative regions of the arteries, representing sites of vascular injury were microdissected, quick-frozen on dry ice, and stored in liquid nitrogen. Uninjured arteries were isolated and analyzed similarly; the entire uninjured artery was frozen. Total RNA was prepared. A 100-ng portion of each sample was subjected to linear amplification and hybridized to Affymetrix mouse gene 1.0ST.
2012-09-10 | E-GEOD-40637 | biostudies-arrayexpress