Balloon injury-induced gene expression in common carotid arteries of wistar rat
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE48279 | GEO | 2013/06/29
SECONDARY ACCESSION(S): PRJNA210000
REPOSITORIES: GEO
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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: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:The proliferation and remodeling of vascular smooth muscle cells (VSMCs) is an important pathological event in atherosclerosis and restenosis. Here we report that microRNA-132 (miR-132) blocks vascular smooth muscle cells (VSMC) proliferation by inhibiting the expression of LRRFIP1 [leucine-rich repeat (in Flightless 1) interacting protein-1]. MicroRNA microarray revealed that miR-132 was upregulated in the rat carotid artery after catheter injury, which was further confirmed by quantitative real-time RT-PCR. Transfection of an miR-132 mimic significantly inhibited the proliferation of VSMCs, whereas transfection of an miR-132 antagomir increased it. Bioinformatics showed that LRRFIP1 is a target candidate of miR-132. miR-132 down-regulated luciferase activity driven by a vector containing the 3’-untranslated region of Lrrfip1 in a sequence-specific manner. LRRFIP1 induced VSMC proliferation. Immunohistochemical analysis revealed that Lrrfip1 was clearly expressed along with the basal laminar area of smooth muscle, and its expression pattern was disrupted 7 days after arterial injury LRRFIP1 mRNA was decreased 14 days after injury. Delivery of miR-132 to rat carotid artery attenuated neointimal proliferation in carotid artery injury models. Our results suggest that miR-132 is a novel regulator of VSMC proliferation that represses neointimal formation by inhibiting LRRFIP1 expression. Balloon injury was induced in the carotid arteries of male Sprague–Dawley rats weighing approximately 250 g. Total RNA were extracted from the arterial sections after 10 days. MicroRNA profile of the sample was compared with non-injured control.
2013-04-23 | E-GEOD-45433 | 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:Affymetrix Mouse Gene 2.0 ST Gene Expression Microarrays were used to analyze differentially expressed genes after carotid artery ligation. The aim of this experiment was to detect genes regulated in Has3 deficient as compared to wildtype controls that might be involved in neointimal hyperplasia. Neointimal hyperplasia was induced in female Has3 deficient mice and wildtype controls by ligation of the left common carotid artery. Carotid transcriptome was analyzed 5 days after surgery in ligated and non-ligated carotid arteries.
2015-11-24 | E-GEOD-70410 | biostudies-arrayexpress
Project description:Balloon injury-induced gene expression in common carotid arteries of wistar rat
| PRJNA210000 | ENA
Project description:To investigate the function and potential mechanism of PARP-1 poly(ADP-ribose) polymerase 1 (PARP1) in diabetic neointimal hyperplasia. Type 1 diabetes mellitus was induced using streptozotocin (STZ) in wild-type mice and PARP1-/- mice, and ligation of the left carotid artery was performed to induce neointimal hyperplasia. Ligated carotid arteries from diabetic mice developed more extensive neointimal hyperplasia and showed greater proliferation and migration than arteries from nondiabetic mice. The augmented remodeling response was absent in diabetic mice deficient in PARP1. PARP1 deficiency reduces diabetic neointimal hyperplasia by upregulating tissue factor pathway inhibitor (TFPI)-2, which acted as a suppressor of vascular smooth muscle cell (VSMCs) proliferation and migration. The underlying mechanisms involve PARP1 that acts as a negative transcription factor by enhancing TFPI-2 promoter DNA methylation. Our studies demonstrated for the first time that Inhibition of PARP1 alleviates neointimal hyperplasia in diabetes by up-regulating TFPI-2 expression and blocking VSMC proliferation and migration. The development of PARP1 inhibitors might serve to limit mainly proliferative and migratory processes in restenosis-prone diabetic patients
2019-11-30 | GSE141193 | GEO
Project description:Bare-metal (BMS) and drug-eluting stents (DES) were implanted in pig coronary arteries with an overstretch during coronary angioplasty under optical coherence tomography guidance. Arteries subjected to plain old balloon angioplasty (POBA) alone served as controls. Stented/balloon dilated segments were harvested 1, 3, 7, 14 and 28 days post-intervention for proteomics analysis. At day 28 all stented arteries showed a neointima formation covering the stent struts. The evolved neointima was separated from the media and analysed in a separate proteomics analysis. In total, 31 samples were analysed for the media by LC-MS/MS (n=3 BMS/DES at each time-point 1, 3, 7 and 28 days; n=4 POBA early [day1-day3] and n=3 POBA late [day 14 - day28]). For the neointima a total of 14 samples were analysed (n=7 BMS, n=7 DES at 28 days) including the neointima of arteries of a second cohort with 4 samples each for BMS and DES day 28. The neointima samples were run in duplicates.
2017-11-24 | PXD005726 | Pride
Project description:Tissue Factor Pathway Inhibitor-2 is Induced by Fluid Shear Stress in Vascular Smooth Muscle Cells and Affects Cell Proliferation and Survival Introduction: Vascular smooth muscle cells (SMCs) are exposed to fluid shear stress (FSS) after interventional procedures such as balloon-angioplasty. Whereas the effects of hemodynamic forces on endothelial cells are explored in detail, the influence of FSS on smooth muscle cell function is poorly characterized. Here, we investigated the effect of FSS on SMC gene expression and function. Methods: Laminar FSS of arterial level (14 dynes/cm2) was applied to SMC cultures for 24 h in a parallel-plate flow chamber. The effect of FSS on gene expression was first screened with microarray technology and the results further verified by real time (RT) PCR and immunoblotting. Protein expression was also studied in the rat carotid artery after balloon-injury and DNA synthesis and apoptosis was examined in SMCs in vitro. Results: Microarrays identified tissue-pathway inhibitor-2 (TFPI-2) as the most differentially expressed gene by FSS in cultured SMCs. The regulatory effect of FSS on the expression of TFPI-2 was confirmed by RT-PCR and immunobloting demonstrating a more than 400-fold increase in TFPI-2 expression in SMCs exposed to FSS compared to static controls and a consistent upregulation at the protein level. Functionally, SMC proliferation was decreased by FSS and recombinant TFPI-2 was found to inhibit SMC proliferation and induce SMC apoptosis as indicated by activation of caspase-3. In vivo, TFPI-2 expression was found to be up-regulated 5, 10 and 20 h after rat carotid balloon-injury and immunohistochemistry demonstrated TFPI-2 protein in luminal SMCs exposed to FSS in rat carotid intimal hyperplasia 10 days after balloon-injury. Conclusion: FSS strongly influence gene expression in cultured SMCs and induce TFPI-2 expression, which is also expressed after rat carotid balloon injury in luminal SMCs exposed to FSS. Functionally, TFPI-2 may play an important role in vessel wall repair by regulating SMC proliferation and survival. Further studies are needed to elucidate the mechanisms by which TFPI-2 control SMC function. 3 x 2 samples from a paired fluid shear stress experiment on smooth muscle cells.
2010-04-12 | E-GEOD-19909 | biostudies-arrayexpress
Project description:Albeit vascular prostheses for the replacement of large arteries (e.g. aorta) are commercially available for decades, small-diameter vascular grafts (e.g., for coronary artery bypass graft surgery) still remain an unmet clinical need. Biostable polymers commonly used for the fabrication of aortic prostheses (e.g., poly(ethylene terephthalate) or expanded poly(tetrafluoroethylene)) have insufficient haemocompatibility to withstand thrombosis at low blood flow characteristic of small arteries (e.g., coronary artery). Hence, researchers endeavor to develop a biodegradable, tissue-engineered vascular graft (TEVG) to avoid the use of autologous blood vessels, such as saphenous vein or internal mammary artery, as conduits during the bypass surgery. Although a number of promising prototypes have been designed to date, none of them passed the pre-clinical trials successfully. Implantation into the ovine or porcine arteries is associated with thrombosis, neointimal hyperplasia, and aneurysms within one-year postoperation, precluding further clinical translation of TEVGs. Among the reasons of such impediment is that pathophysiology of TEVG implantation remains unclear and the molecular events occurring in the TEVG upon its implantation have not been properly investigated hitherto. Here, we for the first time performed a proteomic profiling of the TEVGs (n = 12) implanted into the ovine carotid arteries for one year and suffered from thrombosis to identify the signatures of TEVG failure in an unbiased manner. Contralateral intact ovine carotid arteries (n = 12) have been selected as a control group.
2022-11-26 | PXD036520 | Pride