Effect of vasostatin-2 treatment on gene expression in mouse femoral arteries following wire injury
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PROVIDER: PRJNA1254148 | ENA |
REPOSITORIES: ENA
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Project description:Neointimal hyperplasia is a major pathological process underlying restenosis following vascular injury. Vasostatin-2, a bioactive peptide derived from chromogranin A, has been implicated in vascular protection, but its mechanism remains unclear. To investigate the molecular basis through which vasostatin-2 modulates vascular remodeling, we performed transcriptomic profiling using RNA sequencing in a mouse model of femoral artery wire injury. Mice underwent wire-induced endothelial denudation of the femoral artery and immediately received perivascular treatment with either vasostatin-2 or saline. At 3 days post-injury, the injured femoral arteries were harvested for RNA-seq analysis to examine the impact of vasostatin-2 treatment on gene expression changes associated with vascular injury and neointima formation. This dataset provides insight into the transcriptional programs regulated by vasostatin-2 during the early phase of vascular injury and may reveal therapeutic targets for preventing restenosis.
2025-09-01 | GSE295298 | GEO
Project description:We performed wire-induced injuries in 12 week old C57BL/6J mice. Dilation of the femoral artery was performed by inserting a straight spring wire (0.38 mm diameter) for 10 mm towards the iliac artery, as described previously (Sedding D, Daniel JM, Muhl L, Hersemeyer K, Brunsch H, Kemkes-Matthes B, Braun-Dullaeus RC, Tillmanns H, Weimer T, Preissner KT, Kanse SM. The g534e polymorphism of the gene encoding the factor vii-activating protease is associated with cardiovascular risk due to increased neointima formation. The Journal of experimental medicine. 2006;203:2801-2807). Mice were sacrificed and perfused with phosphate buffered saline via the left ventricle. Femoral arteries were excised at 10 and 21 days after injury, snap-frozen and miRNA was isolated by phenol-chloroform extraction following the purelink
2019-03-05 | GSE111701 | 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
Project description:Differentially regulated miRNAs following murine femoral artery injury
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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: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: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: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:Pathologic and clinical investigations suggest that femoral artery plaques are less inflammatory than other vascular beds, including carotid arteries. However, limited data exist regarding comparative immune landscapes and inflammatory polarization that may underlie such differences in femoral versus carotid plaque.
2023-06-12 | GSE234077 | GEO