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Longitudinal analysis of developing neointimal vascular proliferation and pulmonary hypertension in rats

ABSTRACT: 6 timepoints: Day 0 (normal controls), progressively developing neointimal vascular proliferation and pulmonary hypertension in vehicle treated animals (Days 14, 21, 28 and 35) and triptolide-treated animals at Day 35. Replicates: 6 for Day 0 (normal) 2 for Daty 14 3 each for Days 21, 28, 35 and Triptolide -treated at day 35 (T) Keywords: time-course

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE843 | GEO | 2003/12/02

SECONDARY ACCESSION(S): PRJNA87851

REPOSITORIES: GEO

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Longitudinal analysis of developing neointimal vascular proliferation and pulmonary hypertension in rats

Project description:6 timepoints: Day 0 (normal controls), progressively developing neointimal vascular proliferation and pulmonary hypertension in vehicle treated animals (Days 14, 21, 28 and 35) and triptolide-treated animals at Day 35. Replicates: 6 for Day 0 (normal) 2 for Daty 14 3 each for Days 21, 28, 35 and Triptolide -treated at day 35 (T)

2010-06-05 | E-GEOD-843 | biostudies-arrayexpress

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Deletion of hyaluronan synthase 3 inhibits neointimal hyperplasia

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.

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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, 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

Balloon injury-induced gene expression in common carotid arteries of wistar rat

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Genome-wide transcriptional profiling in relation to seed storage compounds in tetralocular Brassica rapa

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Inhibition of PARP 1 Protects Against Hyperglycemic-induced Neointimal Hyperplasia by Upregulating TFPI-2 Activity

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

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