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Whole-Genome Transcriptome Profiling of Microvascular Free Flaps

ABSTRACT: Vascular compromise in microsurgical free flap transfers continues to present devastating outcomes in terms of flap failure and increased operating room costs. Current devices to detect early venous congestion have not become widely accepted because of insufficient sensitivity, incisiveness, or practicality. In our study, we developed a venous obstruction rat model in which the superficial inferior epigastric (SIE) vessels to the lower abdominal flaps was separated and artery or vein was ligated, and the flap reattached. Flaps were harvested 4 hours post-op. Total RNA was isolated and gene expression profiles were compared by Affymetrix Whole Genome 230 2.0. Flaps from groups of Venous or artery congestion (VC or AC, resp.) and sham operation group, were harvested and RNA extraction and hybridization on Affymetrix microarrays. Other controls including histology assays to assure comparable phenotype within groups.

ORGANISM(S): Rattus norvegicus

SUBMITTER: Yiqiang Zhang

PROVIDER: E-GEOD-35270 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Whole-Genome Transcriptome Profiling of Microvascular Free Flaps

Project description:Vascular compromise in microsurgical free flap transfers continues to present devastating outcomes in terms of flap failure and increased operating room costs. Current devices to detect early venous congestion have not become widely accepted because of insufficient sensitivity, incisiveness, or practicality. In our study, we developed a venous obstruction rat model in which the superficial inferior epigastric (SIE) vessels to the lower abdominal flaps was separated and artery or vein was ligated, and the flap reattached. Flaps were harvested 4 hours post-op. Total RNA was isolated and gene expression profiles were compared by Affymetrix Whole Genome 230 2.0.

2016-07-24 | GSE35270 | GEO

The effect of pressure on gene expression of blood and venous endothelial cells in humans

Project description:Two matched groups of Heart Failure with reduced ejection fraction patients with no peripheral venous congestion were studied: with recent prior heart failure hospitalization vs. without recent heart failure hospitalization. Peripheral venous congestion was modeled by inflating a cuff around the dominant arm, targeting an ~30mmHg increase in venous pressure (venous stress test). Blood and endothelial cells were sampled before and after 90 minutes of venous stress test.

2023-08-28 | GSE237856 | GEO

Renal congestion exacerbates acute kidney injury in mice

Project description:The number of heart failure (HF) patients is increasing. HF is frequently accompanied by kidney dysfunction and such organ failure is closely related. Recent investigations revealed that increased renal venous pressure, rather than decreased cardiac output, causes the deterioration of kidney function in HF patients; however, the underlying responsible mechanisms are unknown. We demonstrated that reduced blood flow speed in peritubular capillaries (PTCs) by renal congestion and upregulation of nuclear factor-κB (NF-κB) signaling synergistically exacerbate kidney injury. We generated a novel mouse model with unilateral renal congestion by coarctation of the inferior vena cava between renal veins. Intravital imaging highlighted the notable dilatation of PTCs and decreased renal blood flow speed in the congestive kidney. Renal damage after ischemia reperfusion injury was exacerbated in the congestive kidney and accumulation of polymorphonuclear leukocytes (PMNs) within PTCs was observed at the acute phase after injury. Pharmacological inhibition of NF-κB ameliorated renal congestion-mediated exacerbation of kidney injury. In vitro, adhesion of PMNs on the TNFα-stimulated endothelial cells was accelerated by perfusion of PMNs at a slower speed, which was cancelled by the inhibition of NF-κB signaling. Our study demonstrates the importance of slower blood flow accompanying activated NF-κB signaling in the congestive kidney in the exacerbation of renal injury. These mechanisms may explain how increased renal venous pressure in HF patients causes the deterioration of kidney dysfunction. Inhibition of NF-κB signaling may be a therapeutic candidate for the vicious cycle between heart and kidney failure with increased renal venous pressure.

2024-02-16 | GSE166838 | GEO

mRNA expression profile in vascular smooth muscle cells (VSMCs) after inducing calcification

Project description:Vascular calcification (VC) is often associated with cardiovascular and metabolic diseases. However, the molecular mechanisms linking VC to these diseases have yet to be elucidated. Here we report that MDM2-induced polyubiquitination of histone deacetylase 1 (HDAC1) mediates VC. Loss of HDAC1 activity via either chemical inhibitor or genetic ablation enhanced VC. HDAC1 protein, but not mRNA, was reduced in cell and animal calcification models and in human calcified coronary artery. In the calcification-provoking condition, proteasomal degradation of HDAC1 preceded VC. The calcification-provoking condition induced MDM2 E3 ligase, which then resulted in HDAC1 K74 polyubiquitination. Overexpression of MDM2 enhanced VC, whereas loss of MDM2 blunted it. Decoy peptides spanning HDAC1 K74 and RG 7112, an MDM2 inhibitor, prevented VC in vivo and in vitro. These results demonstrate a previously unknown ubiquitination pathway and suggest MDM2-mediated HDAC1 polyubiquitination as a new therapeutic target in VC.

2015-11-07 | GSE74755 | GEO

mRNA expression profile in vascular smooth muscle cells (VSMCs) after inducing calcification

2015-11-07 | E-GEOD-74755 | biostudies-arrayexpress

Nr2f1a maintains atrial nkx2.5 expression to repress pacemaker identity within venous atrial cardiomyocytes of zebrafish

Project description:Maintenance of cardiomyocyte identity is vital for normal heart development and function. However, our understanding of cardiomyocyte plasticity remains incomplete. Here, we show that sustained expression of the zebrafish transcription factor Nr2f1a prevents the progressive acquisition of ventricular cardiomyocyte (VC) and pacemaker cardiomyocyte (PC) identities within distinct regions of the atrium. Transcriptomic analysis of flow-sorted atrial cardiomyocytes (ACs) from nr2f1a mutant zebrafish embryos showed increased VC marker gene expression and altered expression of core PC regulatory genes, including decreased expression of nkx2.5, a critical repressor of PC differentiation. At the arterial (outflow) pole of the atrium in nr2f1a mutants, cardiomyocytes resolve to VC identity within the expanded atrioventricular canal. However, at the venous (inflow) pole of the atrium, there is a progressive wave of AC transdifferentiation into PCs across the atrium toward the arterial pole. Restoring Nkx2.5 is sufficient to repress PC marker identity in nr2f1a mutant atria and analysis of chromatin accessibility identified a Nr2f1a-dependent nkx2.5 enhancer expressed in the atrial myocardium directly adjacent to PCs. CRISPR/Cas9-mediated deletion of the putative nkx2.5 enhancer leads to a loss of Nkx2.5-expressing ACs and expansion of a PC reporter, supporting that Nr2f1a limits PC differentiation within venous ACs via maintaining nkx2.5 expression. The Nr2f-dependent maintenance of AC identity within discrete atrial compartments may provide insights into the molecular etiology of concurrent structural congenital heart defects and associated arrhythmias.

2023-05-12 | GSE194054 | GEO

Renal congestion (Rattus)

Project description:Renal congestion (Rattus)

| PRJNA459486 | ENA

Development and validation of VTE prediction model in patients with radical colorectal cancer surgery

Project description:Interventions: Gold Standard:Double lower limb venous color ultrasound, double upper limb venous color ultrasound, pulmonary artery CT angiography;Index test:VTE prediction model in patients with radical colorectal cancer surgery Primary outcome(s): Deep vein thromboembolism;Pulmonary artery embolism Study Design: Cross-sectional

| 38293 | ecrin-mdr-crc

Identification of potential abnormal methylation modified genes in coronary artery ectasia

Project description:Coronary artery ectasia (CAE) is a rare but easily recognized abnormality of coronary artery anatomy and morphology. Up to now, the pathogenesis of CAE remains unclear. Firstly, the peripheral venous blood samples of patients with CAE were obtained for the RNA sequencing to identify differentially expressed genes (DEGs), followed by functional analysis. Secondly, DNA methylation profile in CAE was downloaded from the dataset of GSE87016 to identify differentially methylated genes (DMGs). Lastly, after taking interaction genes between DEGs and DMGs, abnormal methylation modified genes were identified.

2023-09-06 | GSE222041 | GEO

Rat hindlimb arteries: Shunt versus Control

Project description:Arteriogenesis is defined as the development of a collateral circulation, bypassing an arterial occlusion. We have previously demonstrated that chronically elevated fluid shear stress completely normalized blood flow in femoral artery ligated rabbits. This was realized by a surgical intervention: the creation of an arterio- venous anastomosis (shunt) between the femoral artery and the accompanying vein. The aim of this study was a gene profiling approach in order to identify differentially expressed genes during collateral growth in the shunt model when compared to pre-existent collaterals (sham).

2010-05-26 | GSE16359 | GEO

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