Alteration of mRNA and microRNA expression profiles in rat muscular type vasculature in early postnatal development [miRNA]
Ontology highlight
ABSTRACT: This study tested the hypothesis that miRNA expression profiles change in the muscular type rat saphenous artery during early postnatal development. To explore this, we performed miRNA microarray analysis on muscular type saphenous arteries of young (10-12 days) and adult (2-3 months) rats. For one sample four saphenous arteries from 2 young animals (n = 4 samples per group) or two saphenous arteries from one adult animal (n = 4 samples per group) were used to profile miRNA (n = 8; GeneChip® miRNA 3.0) expression changes during the muscular type rat saphenous artery during early postnatal development. In this study, 10-12 days old (“young”) and 2 - 3 months old (“adult”) male Wistar rats were used.
Project description:This study tested the hypothesis that miRNA expression profiles change in the muscular type rat saphenous artery during early postnatal development. To explore this, we performed miRNA microarray analysis on muscular type saphenous arteries of young (10-12 days) and adult (2-3 months) rats.
Project description:This study tested the hypothesis that mRNA expression profiles change in the muscular type rat saphenous artery during early postnatal development. To explore this, we performed mRNA microarray analysis on muscular type saphenous arteries of young (10-12 days) and adult (2-3 months) rats. For one sample four saphenous arteries from 2 young animals (n = 4 samples per group) or two saphenous arteries from one adult animal (n = 4 samples per group) were used to profile mRNA (n = 8; GeneChip® Rat Gene 1.0) expression changes during the muscular type rat saphenous artery during early postnatal development. In this study, 10-12 days old (“young”) and 2 - 3 months old (“adult”) male Wistar rats.
Project description:This study tested the hypothesis that mRNA expression profiles change in the muscular type rat saphenous artery during early postnatal development. To explore this, we performed mRNA microarray analysis on muscular type saphenous arteries of young (10-12 days) and adult (2-3 months) rats.
Project description:Transcriptional profiling from young, old, healthy, or injured rat iliac arteries. We studied the gene expression profile in a model of mechanical vascular injury in the iliac artery of aging (22 months old) and young rats (4 months old). We investigated aging-related variations in gene expression at 30 min, 3d and 7d post injury.
Project description:We investigated morphometric structure and gene expression by microarray analysis in a small diameter artery, branch of the saphenous artery (a resistance artery), in representative models of renin-angiotensin system (RAS)-dependent and glucocorticoid hypertension, using the spontaneously hypertensive rat (SHR) and adrenocorticotropic hormone (ACTH)-induced hypertensive rat, respectively. Sixteen-week-old male Wistar-Kyoto (WKY) and age-matched spontaneously hypertensive rats (SHR) were used. Keywords: Comparison of global gene expression in resistance arteries of normotensive and genetically hypertensive rats and ACTH-treated rats.
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.
Project description:Using the Illumina Infinium Human Methylation27 BeadChip, we performed a genome-wide analysis of DNA methylation in right coronary artery in the area of advanced atherosclerotic plaques, atherosclerotic-resistant internal mammary arteries, and great saphenous veins obtained from same patients with coronary heart disease. The resulting DNA methylation patterns were markedly different between all the vascular tissues. The genes hypomethylated in athero-prone arteries to compare with atherosclerotic-resistant arteries were predominately involved in regulation of inflammation and immune processes, as well as development. The great saphenous veins exhibited an increase of the DNA methylation age in comparison to the internal mammary arteries. Gene ontology analysis for genes harboring hypermethylated CpG-sites in veins revealed the enrichment for biological processes associated with the development. Four CpG-sites located within the MIR10B gene sequence and about 1 Kb upstream of the HOXD4 gene were also confirmed as hypomethylated in the independent dataset of right coronary arteries in the area of advanced atherosclerotic plaques in comparison with the other vascular tissues. Bisulfite converted genomic DNA from 24 samples was denatured, whole-genome amplified, fragmented and subsequently hybridized to the Illumina Infinium 27k Human Methylation Beadchip.
Project description:Using the Illumina Infinium Human Methylation27 BeadChip, we performed a genome-wide analysis of DNA methylation in right coronary artery in the area of advanced atherosclerotic plaques, atherosclerotic-resistant internal mammary arteries, and great saphenous veins obtained from same patients with coronary heart disease. The resulting DNA methylation patterns were markedly different between all the vascular tissues. The genes hypomethylated in athero-prone arteries to compare with atherosclerotic-resistant arteries were predominately involved in regulation of inflammation and immune processes, as well as development. The great saphenous veins exhibited an increase of the DNA methylation age in comparison to the internal mammary arteries. Gene ontology analysis for genes harboring hypermethylated CpG-sites in veins revealed the enrichment for biological processes associated with the development. Four CpG-sites located within the MIR10B gene sequence and about 1 Kb upstream of the HOXD4 gene were also confirmed as hypomethylated in the independent dataset of right coronary arteries in the area of advanced atherosclerotic plaques in comparison with the other vascular tissues.
Project description:We investigated morphometric structure and gene expression by microarray analysis in a small diameter artery, branch of the saphenous artery (a resistance artery), in representative models of renin-angiotensin system (RAS)-dependent and glucocorticoid hypertension, using the spontaneously hypertensive rat (SHR) and adrenocorticotropic hormone (ACTH)-induced hypertensive rat, respectively. Sixteen-week-old male Wistar-Kyoto (WKY) and age-matched spontaneously hypertensive rats (SHR) were used. Experiment Overall Design: There were 3 experimental groups: Group 1: 16-week male Wistar-Kyoto rats; Group 2: 16-week male Wistar-Kyoto rats treated with ACTH (0.1mg/kg/day) subcutaneously, for 4 weeks prior to sampling (i.e. during weeks 12-16 of life) ; Group3: 16-week male SHR (spontaneously hypertensive) rats. There were 3 replicate hybridizations in each experimental group. Due to the low yield of total RNA obtained from the arterial sections, each replicate was composed of RNA pooled from 2-3 different rats.
Project description:Background: The vascular wall of small arteries is heavily affected by high blood pressure. However, the underlying mechanisms causing vascular changes are not fully elucidated. Using a novel data-independent acquisition mass spectrometry (DIA-MS) approach, we aimed to determine the proteomic changes in small mesenteric arteries during early-onset high blood pressure in a rat model of hypertension. Methods: Snap frozen small mesenteric and renal arteries from the spontaneous hypertension rat (SHR) model and Wistar Kyoto (WKY) control rats were collected from two time points (6- and 12-weels of age) and analyzed by a label free quantitative DIA-MS workflow. Mesenteric arteries from Wister Hannover rats were included as an additional control to clarify genetic drift caused by selective inbreeding. Results: We identified a total of 3956 consistent proteins in the mesenteric artery wall and found that 286 proteins were significantly regulated in 12-weeks old SHRs compared to WKY controls. Comparing to an in silico matrisome database, we identified 38 extracellular matrix-associated proteins that could distinguish SHRs from WKY controls. Furthermore, when comparing the significantly regulated proteins identified in mesenteric and renal arteries, we identified 18 proteins, including Serpina3l, Igg-2a, ENSRNOG00000049829, Acyp2, Enpp3, Lss, Acaa1a, Basp1, an isoform of Basp1, Flot1, Flot2, Gstt1, Nit1, Ppid, Ikbkap, Poglut3, P4ha2 and Usp15, that were changed in both vascular beds. These proteins were associated with vital cellular processes, such as dyslipidemia, protease inhibition, remodeling and generation of reactive oxygen species. Majority of the identified proteins and pathways were associated with hypertension, and mapping the underlying changes help understanding the pathological processes occurring in the arterial wall during early-onset hypertension. Conclusions: Our data provides an in-depth analysis of the proteomic architecture of the mesenteric and renal artery wall from SHRs and WKY control rats. We identified 18 novel candidate proteins that highlights critical changes in small arteries of the SHR.