Microarray analysis of femoral artery injury in mice
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ABSTRACT:
ORGANISM(S): synthetic construct Mus musculus
PROVIDER: GSE40637 | GEO | 2012/09/10
SECONDARY ACCESSION(S): PRJNA174444
REPOSITORIES: GEO
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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:Rapid regeneration of smooth muscle after vascular injury is essential for maintaining proper artery function. The current view holds that pre-existing smooth muscle proliferate and expand in responding to vascular injury, contributing to virtually all new smooth muscle cells. Whether resident vascular stem cells for smooth muscle exist remains controversial and their putative functional role for artery repair and regeneration is elusive. Here we performed cell fate mapping and single cell RNA sequencing to identify Sca1+ vascular stem cells (VSCs) residing in the adventitial layer of artery wall.
2019-12-27 | GSE139827 | 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:Differentially regulated miRNAs following murine femoral artery injury
| PRJNA437910 | ENA
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:Acute vascular injury is an unwelcome consequence of invasive treatments designed to alleviate symptoms of vascular stenosis. Resulting fibrotic scarring and neointima formation may result in loss of lumen diameter and diminished vascular function. Understanding of the key phases of acute inflammation, resolution and remodeling has the potential to minimise unwanted effects on the vasculature and therefore improve patient outcomes. The cellular landscape of blood vessels is highly hetergeneous in nature, and therefore data at single-cell resolution is of high relevance to this problem. Herein, the cellularity of murine carotid artery tissue is described in a cell- and time-resolved manner. Single-cell RNA-sequencing of carotid tissue isolated at time-points ranging from uninjured vessel to 14 days post-injury enabled the recapitulation of all stages of vascular injury. In these data, a sub-population of smooth muscle cells which also arises in atherosclerosis and myocardial infarction was identified. So-called stem cells/endothelial cells/monocytes (SEM) cells are candidates for repopulating injured vessels, and were amongst the most proliferative cell clusters following wire-injury of the carotid artery. Transcriptional signatures reflecting SEM gene expression patterns could also be detected in bulk RNA-sequencing of neointimal tissue isolated by laser capture microdissection. These data indicate that phenotypic plasticity of smooth muscle cells is highly important to the progression of lumen loss following acute vascular insult.
2023-03-09 | GSE217801 | GEO
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.
2013-04-23 | GSE45433 | GEO
Project description: Not available
| S-EPMC6287226 | biostudies-literature
Project description:Endothelial cells play a critical role in multiple cardiovascular diseases. CD34+ cells are believed to be endothelial progenitors that have been used to treat cardiovascular disease. However, the exact identity and the role of CD34+ cells in vascular regeneration remains unclear.Here we performed single cell RNA sequencing to identify heterogeneous CD34+ cells serve as a contributor to endothelial regeneration.
2021-10-13 | GSE182232 | GEO
Project description:Surgical interventions on blood vessels bear a risk for intimal hyperplasia and atherosclerosis as a consequence of injury. A specific feature of intimal hyperplasia is the loss of vascular smooth muscle cell (VSMC) differentiation gene expression. We hypothesized that immediate responses following injury induce vascular remodeling. To differentiate injury due to trauma, reperfusion and pressure changes we analyzed vascular responses to carotid artery bypass grafting in mice compared to transient ligation. As a control, the carotid artery was surgically laid open only. In both, bypass or ligation models, the inflammatory responses were transient, peaking after 6h, whereas the loss of VSMC differentiation gene expression persisted. Extended time kinetics showed that transient carotid artery ligation was sufficient to induce a persistent VSMC phenotype change throughout 28 days. Transient arterial ligation in ApoE knockout mice resulted in atherosclerosis in the transiently ligated vascular segment but not on the not-ligated contralateral side. The VSMC phenotype change could not be prevented by anti-TNF antibodies, Sorafenib, Cytosporone B or N-acetylcysteine treatment. Surgical interventions involving hypoxia/reperfusion are sufficient to induce VSMC phenotype changes and vascular remodeling. In situations of a perturbed lipid metabolism this bears the risk to precipitate atherosclerosis.
2018-09-06 | GSE119549 | GEO