Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RhoBTB1 Reverses Established Arterial Stiffness in Angiotensin II Hypertension

ABSTRACT: RhoBTB1 Reverses Established Arterial Stiffness in Angiotensin II Hypertension

PROVIDER: PRJNA781123 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR16963108_1.fastq.gz	Fastqsanger.gz
	SRR16963108_2.fastq.gz	Fastqsanger.gz
	SRR16963109_1.fastq.gz	Fastqsanger.gz
	SRR16963109_2.fastq.gz	Fastqsanger.gz
	SRR16963110_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 80

Similar Datasets

RhoBTB1 Reverses Established Arterial Stiffness in Angiotensin II Hypertension

Project description:We are investigating of role of RhoBTB1 in vascular smooth muscle cells. Restoring RhoBTB1 expression in mouse aorta reversed the established arterial stiffness but not hypertension caused by angiotensin II (Ang-II). To investigate the underlying mechanism by which RhoBTB1 reversed arterial stiffness, we performed bulk RNA-sequencing using aorta from four groups: control /RhoBTB1 transgenic mice treated with/without Ang-II.

2022-04-08 | GSE189003 | GEO

RhoBTB1 reverses established arterial stiffness in angiotensin II-induced hypertension by promoting actin depolymerization.

Project description:Arterial stiffness predicts cardiovascular disease and all-cause mortality, but its treatment remains challenging. Mice treated with angiotensin II (Ang II) develop hypertension, arterial stiffness, vascular dysfunction, and a downregulation of Rho-related BTB domain-containing protein 1 (RhoBTB1) in the vasculature. RhoBTB1 is associated with blood pressure regulation, but its function is poorly understood. We tested the hypothesis that restoring RhoBTB1 can attenuate arterial stiffness, hypertension, and vascular dysfunction in Ang II-treated mice. Genetic complementation of RhoBTB1 in the vasculature was achieved using mice expressing a tamoxifen-inducible, smooth muscle-specific RhoBTB1 transgene. RhoBTB1 restoration efficiently and rapidly alleviated arterial stiffness but not hypertension or vascular dysfunction. Mechanistic studies revealed that RhoBTB1 had no substantial effect on several classical arterial stiffness contributors, such as collagen deposition, elastin content, and vascular smooth muscle remodeling. Instead, Ang II increased actin polymerization in the aorta, which was reversed by RhoBTB1. Changes in the levels of 2 regulators of actin polymerization, cofilin and vasodilator-stimulated phosphoprotein, in response to RhoBTB1 were consistent with an actin depolymerization mechanism. Our study reveals an important function of RhoBTB1, demonstrates its vital role in antagonizing established arterial stiffness, and further supports a functional and mechanistic separation among hypertension, vascular dysfunction, and arterial stiffness.

| S-EPMC9090250 | biostudies-literature

Gut microbial composition and functional capacity in patients with arterial stiffness

Project description:Gut microbiota linked to arterial stiffness

| PRJEB49672 | ENA

Transcription profiling of human aortic biopsy samples having differing degrees of stiffness

Project description:BACKGROUND: Previous genomic studies with human tissues have compared differential gene expression between 2 conditions (ie, normal versus diseased) to identify altered gene expression in a binary manner; however, a potentially more informative approach is to correlate the levels of gene expression with quantitative physiological parameters. METHODS AND RESULTS: In this study, we have used this approach to examine genes whose expression correlates with arterial stiffness in human aortic specimens. Our data identify 2 distinct groups of genes, those associated with cell signaling and those associated with the mechanical regulation of vascular structure (cytoskeletal-cell membrane-extracellular matrix). Although previous studies have concentrated on the contribution of the latter group toward arterial stiffness, our data suggest that changes in expression of signaling molecules play an equally important role. Alterations in the profiles of signaling molecules could be involved in the regulation of cell cytoskeletal organization, cell-matrix interactions, or the contractile state of the cell. CONCLUSIONS: Although the influence of smooth muscle contraction/relaxation on arterial stiffness could be controversial, our provocative data would suggest that further studies on this subject are indicated.<br><br>Note that files GSM6179.txt and GSM6182.txt as imported from GEO are identical.

2007-12-13 | E-GEOD-420 | biostudies-arrayexpress

Aortic stiffness

2003-08-28 | GSE420 | GEO

Role of Fibulin-V (FibV) in disturbed flow induced arterial stiffening and atherosclerosis

Project description:The mechanisms of arterial stiffness (independent cardiovascular risk factor) are not well understood. Here, we investigated the role of Fibulin V in arterial stiffness and remodeling in response to disturbed blood flow.

2024-10-01 | GSE222583 | GEO

Disturbed flow promotes arterial stiffening through thrombospondin-1 (TSP-1) signaling pathways

Project description:Arterial stiffness is a prevalent, independent cardiovascular risk factor, but the underlying mechanisms are not well understood. Wall shear stress and shear-sensitive genes may promote arterial stiffening through clinically important signaling pathways. Our goal was to identify how disturbed blood flow leads to arterial stiffness using the mouse partial carotid ligation model. Here we used our in vivo partial carotid ligation model to induce d-flow in the LCA while the contralateral RCA continues to experience stable laminar flow using the C57BL/6x129SvEv mice, TSP-1 knockout (KO), and C57Bl/6J mice. We compared these to aged (80 week) mice which had increased arterial stiffness due to aging. Changes in gene expression were identified using microarrays that were performed on the endothelial-enriched RNA isolated from the carotids exposed to stable flow (RCA) and compared to disturbed flow (LCA). Arterial stiffness was determined ex vivo by biaxial mechanical testing and in vivo by ultrasound techniques. Myointimal hyperplasia and immunohistochemistry were performed in sectioned carotid arteries. In vitro testing of signaling pathways utilized oscillatory and laminar wall shear stress. Human arteries were tested ex vivo to validate critical results found in the animal model.

2017-09-01 | GSE87199 | GEO

Arterial stiffness and cardiac dysfunction in Hutchinson-Gilford Progeria Syndrome corrected by inhibition of Lysyl Oxidase

Project description:Purpose: Arterial stiffening is a hallmark of premature aging in Hutchinson-Gilford Progeria Syndrome (HGPS), but the molecular regulators remain unknown. Here, we show that the LMNAG609G mouse model of HGPS recapitulates the premature arterial stiffening seen in human HGPS. To gain a better understanding of potential stiffness-regulators in LMNAG609G mice, we performed RNA-sequencing analysis on cleaned descending aortas from 2- and 24-month WT and 2-month LMNAG609G mice on a C57BL6 background. Methods: Descending aortas containing the intimal, medial and adventitial layers were isolated from 2- and 24-month male WT and 2-month HGPS mice, and RNA was extracted using the RNeasy Plus Micro kit (Qiagen 74034). The high-throughput library was prepared using the TruSeq stranded total RNA (ribo-Zero) kit (Illumina 20037135). Paired-end sequencing was performed on a HiSeq4000 Sequencing System (Illumina) and generated 14-30 million reads/sample.

2021-02-09 | GSE165409 | GEO

Toll-like receptor 4 deletion partially protects mice from high fat diet-induced arterial stiffness despite the development of gut dysbiosis

Project description:TLR4 knockout mice partially protected from arterial stiffness.

| PRJEB61188 | ENA

Renin-angiotensin system inhibition reverses the altered triacylglycerol metabolic network in diabetic kidney disease

Project description:Renin-angiotensin system inhibition reverses the altered triacylglycerol metabolic network in diabetic kidney disease

| PRJNA594364 | ENA