Renal congestion (Rattus)
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA459486 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We created a rat renal congestion model and investigated the effect of renal congestion on hemodynamics and molecular mechanisms. The inferior vena cava (IVC) between the renal veins was ligated by suture in male Sprague-Dawley rats to increase upstream IVC pressure and induce congestion in the left kidney only. Left kidney congestion reduced renal blood flow, glomerular filtration rate, and increased renal interstitial hydrostatic pressure. Tubulointerstitial and glomerular injury and medullary thick ascending limb hypoxia were observed only in the congestive kidneys. Molecules related to extracellular matrix expansion, tubular injury, and focal adhesion were upregulated in microarray analysis. Renal decapsulation ameliorated the tubulointerstitial injury. Electron microscopy captured pericyte detachment in the congestive kidneys. Transgelin and platelet-derived growth factor receptors, as indicators of pericyte-myofibroblast transition, were upregulated in the pericytes and the adjacent interstitium. With the compression of the peritubular capillaries and tubules, hypoxia and physical stress induce pericyte detachment, which could result in extracellular matrix expansion and tubular injury in renal congestion.
2018-11-14 | GSE114031 | GEO
Project description:Epidemiological studies showed that patients with heart failure frequently develop kidney dysfunction, called cardio-renal syndrome (CRS). Elevated central venous pressure rather than low cardiac output strongly correlates with worsening renal function, and is being increasingly recognized as the pathophysiology responsible for CRS. However, due to the lack of appropriate animal models, the molecular mechanisms underlying the congestion-mediated acceleration of kidney injury, called renal congestion, remain unclear. In the present study, using a novel mouse renal congestion model, we detected injured tubule-specific cell-cell interactions in congestive kidneys and showed that Cellular Communication Network Factor 1 (CCN1) played an important role in this process. Transcriptomics of kidneys with ischemia-reperfusion injury (IRI) and renal congestion revealed the up-regulation of paracrine chemokine-related pathways. The up-regulation of CCN1 was observed in the acute phase after kidney injury with renal congestion. Positive staining for phosphorylated focal adhesion kinase (pFAK), a downstream signaling molecule of CCN1, was noted in fibroblasts at injury sites in congestion-IRI kidneys. CCN1 activated the phosphorylation of FAK and ERK in vitro, which accelerated the migration of fibroblasts and macrophages. We then examined the effects of CCN1 deletion in tubular epithelia on congestion-mediated kidney injury in vivo. pFAK expression in injury sites was down-regulated in CCN1-KO mice, and the congestion-mediated worsening of tissue fibrosis was significantly ameliorated. In conclusion, we herein demonstrated the important role of injured tubule-derived CCN1 on pFAK-mediated fibroblast migration in congestive kidneys. The inhibition of CCN1 has potential as a therapeutic candidate for preventing the transition of renal congestion-mediated kidney injury to fibrosis.
2025-07-09 | GSE283859 | GEO
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
Project description:Renal congestion exacerbates acute kidney injury in mice
| PRJNA702099 | ENA
Project description:We report the difference of mRNA and Long-non-coding RNA state between normal and irradiated skin of rattus
2016-12-31 | GSE86252 | GEO
Project description:Deep sequencing of mRNA from Spalax galili and Rattus norvegicus
2014-06-05 | GSE49485 | GEO
Project description:SISE affect Rattus norvegicus renal Transcriptome
| PRJNA478465 | ENA