Browse
Submit Data
Databases
API
Help

Dataset Information

28 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Oxidative Stress Mediates Vascular Tortuosity.

ABSTRACT: Vascular tortuosity is associated with various disorders and is being increasingly detected through advances in imaging techniques. The underlying mechanisms for vascular tortuosity, however, remain unclear. Here, we tested the hypothesis that oxidative stress mediates the generation of tortuous vessels. We used the bilateral common carotid artery (CCA) ligation model to induce vascular tortuosity. Both young and adult rats showed basilar artery tortuous morphological changes one month after bilateral CCA ligation. These tortuous changes were permanent but more pronounced in the adult rats. Microarray and real-time PCR analysis revealed that these tortuous changes were accompanied by the induction of oxidative stress-related genes. Moreover, the indicated model in rabbits showed that tortuous morphological changes to the basilar artery were suppressed by antioxidant treatment. These results are highly suggestive of the significance of oxidative stress in the development of vascular tortuosity. Although further studies will be needed to elucidate the possible mechanisms by which oxidative stress enhances vascular tortuosity, our study also points toward possible prophylaxis and treatment for vascular tortuosity.

SUBMITTER: Fumoto T

PROVIDER: S-EPMC8228074 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Similar Datasets

Neutrophil oxidative stress mediates obesity-associated vascular inflammation and metastatic transmigration

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-01-25 | GSE165443 | GEO

Gene expression changes accompanying vascular tortuosity

Project description:To gain insight into vascular tortuosity, we analyzed gene expression in normal and tortuous vessels. We induced vascular tortuosity in basilar artery using bilateral common carotid artery ligation in One-year old SD rats. Four weeks after the ligation, total RNA was extracted. Equal amounts of RNA from four rats were pooled and 50 ng RNA was subjected to microarray analysis. Pooled RNA from four Sham operated rats were used as a control.

2021-05-15 | GSE174455 | GEO

m6A Modification Mediates Endothelial Cell Responses to Oxidative Stress in Vascular Aging Induced by Low Fluid Shear Stress.

Project description:N6-methyladenosine (m6A) is one of the most prevalent, abundant, and internal transcriptional modification and plays essential roles in diverse cellular and physiological processes. Low fluid shear stress (FSS) is a key pathological factor for many cardiovascular diseases, which directly forces on the endothelial cells of vessel walls. So far, the alterations and functions of m6A modifications in vascular endothelial cells at the low FSS are still unknown. Herein, we performed the transcriptome-wide m6A modification profiling of HUVECs at different FSS. We found that the m6A modifications were altered earlier and more sensitive than mRNA expressions in response to FSS. The low FSS increased the m6A modifications at CDS region but decreased the m6A modifications at 3' UTR region and regulated both the mRNA expressions and m6A modifications of the m6A regulators, such as the RBM15 and EIF3A. Functional annotations enriched by the hypermethylated and hypomethylated genes at low FSS revealed that the m6A modifications were clustered in the aging-related signaling pathways of mTOR, PI3K-AKT, insulin, and ERRB and in the oxidative stress-related transcriptional factors, such as HIF1A, NFAT5, and NFE2L2. Our study provided a pilot view of m6A modifications in vascular endothelial cells at low FSS and revealed that the m6A modifications driven by low FSS mediated the cellular responses to oxidative stress and cell aging, which suggested that the m6A modifications could be the potential targets for inhibiting vascular aging at pathological low FSS.

| S-EPMC9897929 | biostudies-literature

Neutrophil oxidative stress mediates obesity-associated vascular inflammation and metastatic transmigration (Neutrophils_RNA-seq)

Project description:Obesity is linked to greater cancer incidence and mortality across multiple tumor types. In breast cancer, metastasis is the leading cause of cancer-related deaths, and epidemiological studies have shown that obesity is associated with increased breast cancer metastasis to lung and liver. Using both diet-induced and genetic preclinical models of obesity, it was previously shown that obese adipose tissue systemically induces lung neutrophilia, which is associated with enhanced breast cancer metastasis to this site. Here we performed RNAseq on neutrophils isolated on the lungs from lf vs hf mice.

2021-01-25 | GSE165442 | GEO

Neutrophil oxidative stress mediates obesity-associated vascular inflammation and metastatic transmigration (Endothelial_Cells_RNA-seq)

2021-01-25 | GSE165441 | GEO

Accuracy of vascular tortuosity measures using computational modelling.

Project description:Severe coronary tortuosity has previously been linked to low shear stresses at the luminal surface, yet this relationship is not fully understood. Several previous studies considered different tortuosity metrics when exploring its impact of on the wall shear stress (WSS), which has likely contributed to the ambiguous findings in the literature. Here, we aim to analyze different tortuosity metrics to determine a benchmark for the highest correlating metric with low time-averaged WSS (TAWSS). Using Computed Tomography Coronary Angiogram (CTCA) data from 127 patients without coronary artery disease, we applied all previously used tortuosity metrics to the left main coronary artery bifurcation, and to its left anterior descending and left circumflex branches, before modelling their TAWSS using computational fluid dynamics (CFD). The tortuosity measures included tortuosity index, average absolute-curvature, root-mean-squared (RMS) curvature, and average squared-derivative-curvature. Each tortuosity measure was then correlated with the percentage of vessel area that showed a < 0.4 Pa TAWSS, a threshold associated with altered endothelial cell cytoarchitecture and potentially higher disease risk. Our results showed a stronger correlation between curvature-based versus non-curvature-based tortuosity measures and low TAWSS, with the average-absolute-curvature showing the highest coefficient of determination across all left main branches (p < 0.001), followed by the average-squared-derivative-curvature (p = 0.001), and RMS-curvature (p = 0.002). The tortuosity index, the most widely used measure in literature, showed no significant correlation to low TAWSS (p = 0.86). We thus recommend the use of average-absolute-curvature as a tortuosity measure for future studies.

| S-EPMC8764056 | biostudies-literature

Gene expression changes accompanying vascular tortuosity

Project description:Gene expression changes accompanying vascular tortuosity

| PRJNA729994 | ENA

Oxidative stress mediates an increased formation of vascular endothelial growth factor in human hepatocarcinoma cells exposed to erlotinib.

Project description:The tyrosine kinase inhibitor erlotinib targets the receptor of epidermal growth factor (EGFR) involved in development of hepatocellular carcinoma (HCC). Although inefficient in established HCC, erlotinib has been recently proposed for HCC chemoprevention. Since Cyp3A4 and Cyp1A2 enzymes metabolize erlotinib in the liver, the insights into the mechanisms of erlotinib effects on liver cells with maintained drug metabolizing activity are needed. We applied erlotinib to both commercially available (SNU398, Huh7) and established in Austria HCC cell lines (HCC-1.2, HCC-3). Cyp3A4 and Cyp1A2, microarray gene expression, cell viability, LDH release, DHFC fluorescence were assessed. VEGF expression was analysed by real-time RT-PCR and ELISA. Higher cumulative expression of erlotinib metabolizing enzymes was observed in HCC-1.2 and HCC-3 cells. Gene expression microarray analysis showed upregulation of VEGF signalling by erlotinib. VEGF was increased up to 134 ± 14% (n = 5, p = 0.002) in HCC-1.2, HCC-3 and Huh7 cells. Interventions by Cyp1A2 and Mek2siRNA, MEK inhibitor UO126, diphenylene iodonium, as well as a combination of N-acetylcysteine with selenium all inhibited VEGF upregulation caused by erlotinib. Thus, erlotinib increases VEGF production by mechanisms involving Cyp1A2, oxidative stress and MEK1/2. VEGF may favour angiogenesis and growth of early HCC tumours limiting the therapeutic and chemopreventive effects of erlotinib.

| S-EPMC5593629 | biostudies-literature

Oxidative stress and microRNAs in vascular diseases.

Project description:Oxidative stress has been demonstrated to play a causal role in different vascular diseases, such as hypertension, diabetic vasculopathy, hypercholesterolemia and atherosclerosis. Indeed, increased reactive oxygen species (ROS) production is known to impair endothelial and vascular smooth muscle cell functions, contributing to the development of cardiovascular diseases. MicroRNAs (miRNAs) are non-coding RNA molecules that modulate the stability and/or the translational efficiency of target messenger RNAs. They have been shown to be modulated in most biological processes, including in cellular responses to redox imbalance. In particular, miR-200 family members play a crucial role in oxidative-stress dependent endothelial dysfunction, as well as in cardiovascular complications of diabetes and obesity. In addition, different miRNAs, such as miR-210, have been demonstrated to play a key role in mitochondrial metabolism, therefore modulating ROS production and sensitivity. In this review, we will discuss miRNAs modulated by ROS or involved in ROS production, and implicated in vascular diseases in which redox imbalance has a pathogenetic role.

| S-EPMC3794730 | biostudies-literature

Neutrophil oxidative stress mediates obesity-associated vascular inflammation and metastatic transmigration

Project description:Neutrophil oxidative stress mediates obesity-associated vascular inflammation and metastatic transmigration

| PRJNA694623 | ENA