Differently expressed genes of the heart from sham and 5/6 nephrectomy mice
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ABSTRACT: To examine genome wide transcriptional changes in the heart of 5/6 nephrectomy CKD mice, we performed microarray analysis using the Affymetrix Clariom S array.
Project description:High incidence of heart failure (HF) is a typical characteristic of chronic kidney disease (CKD). However, the pathogenesis of CKD-associated HF remains elusive. Here, we investigated the changes in myocardial energy metabolism in CKD mice and explored the underlying mechanisms. To examine genome wide transcriptional changes in the heart of CKD mice, we performed microarray analysis using the Affymetrix Clariom S mouse.
Project description:Transcriptome analysis was done after warm renal ischemia-reperfusion injury (IRI) in a rat model. Earlier studies have shown a protective effect of prior unilateral nephrectomy (UNx) against IRI in the remaining, contralateral kidney compared to a non-neprectomized control group. We aimed at identifying the underlying molecular mechanisms. We used the Affymetrix Clariom D array (formerly known as RTA 1.0 st.) Array data was processed in the Affymetrix Console Software.
Project description:Kidneys have a limited ability to self-repair, and their response to injury not seldomly leads to chronic kidney disease (CKD). An intriguing phenomenon of successful recovery is observed in models of unilateral acute kidney injury (AKI) upon contralateral nephrectomy. Here we aimed to better understand the cellular mechanisms of this enhanced reparative effect.In a time-course study with different nephrectomy delay times, we found that the most effective rescue after injury was observed when contralateral nephrectomy was performed early during AKI in both rats and mice. This timely intervention led to full functional recovery and attenuation of tubular atrophy, fibrosis, and inflammation, averting AKI-to-CKD transition. Morphometry of histopathology using pathomics revealed distinct trajectories of structural alterations of kidney tubules, distinguishing between atrophy and repair, as adaptive signatures. These responses were corroborated by transcriptomics analysis, which indicated improved cellular energy metabolism after nephrectomy. Lineage tracing of tubular progenitor cells showed that nephrectomy robustly stimulated their clonal expansion, surpassing the levels observed during spontaneous self-repair. Live cell cycle/DNA-content analysis of tubular cells demonstrated a robust polyploid response immediately after the ischemic insult, and revealed that nephrectomy attenuated long term tubular cell polyploidization, a contributor to CKD. Altogether, our data revealed that early timing of nephrectomy in experimental AKI induces an efficient repair response, involving tubular epithelial regeneration while counteracting the progression towards CKD.
Project description:Chronic kidney disease (CKD) is a very important problem in global health treatment. CKD increases the disease risk of apoplexy, cardiac failure and cardiac infarction. Cardiovascular disease is especially the most serious problem. In this study, the expression of mRNA in 5/6 nephrectomy (5/6Nx) mouse splenic monocytes was investigated.
Project description:Chronic kidney disease (CKD) is a very important problem in global health treatment. CKD increases the disease risk of apoplexy, cardiac failure and cardiac infarction. Cardiovascular disease is especially the most serious problem. In this study, the expression of mRNA in 5/6 nephrectomy (5/6Nx) mouse splenic monocytes was investigated.
Project description:Renal gene expression analysis was performed in mouse strains with different propensity to develop progressive chronic kidney disease (CKD) after subtotal nephrectomy: the FVB strain which is spontaneously highly predisposed to CKD and the C57BL/6 which is spontaneously not predisposed to CKD. Subtotal nephrectomy (Nx) is normally initially compensated by proliferative tissue repair (2 days after nephrectomy). After this initial proliferation follows a quiescent period (28 days after NX). Finally, specifically in the sensitive strain there is lesion onset (53 days after Nx). Gene expression was monitored on RNA from whole kidneys from different mouse strains Sham operated or Nephrectomised at three different time-points.
Project description:Rats (Sprague-Dawley) were allotted to subtotal nephrectomy (SNX) or sham (sham) operation. After 2 and 12 weeks the experiment was terminated. RNA was isolated from small pieces of the hearts.
Project description:Chronic kidney disease (CKD) is a very important problem in global health treatment. CKD increases the disease risk of apoplexy, cardiac failure and cardiac infarction. Cardiovascular disease is especially the most serious problem. In this study, the expression of mRNA in the cardiac ventricre prepared from 5/6 nephrectomy (5/6Nx) mouse was investigated.
Project description:Chronic kidney disease (CKD) is a very important problem in global health treatment. CKD increases the disease risk of apoplexy, cardiac failure and cardiac infarction. In addition, neurological complications, including depression and restless legs syndrome, occur in almost all CKD patients; however, the mechanisms of these neurological complications remain unclear. Here, we showed the disruptive effect of chronic renal failure in 5/6 nephrectomy mice on an immobility time of forced swim and tail suspension test and the 24-hr rhythm of Drd2 and clock gene expressions in the striatum. These disruptive effects were induced by abnormal signal transduction in high TGF-M-NM-21 expression from the kidney. Abnormal TGF-M-NM-2 signal in the striatum led to TCF7L2 expression and ID2 induced by TCF7L2 led to disruption of the 24-hr rhythm of clock gene expression. These findings suggest that neurological complications in CKD might be overcome by amelioration of the TGF-M-NM-2 signal. Differential gene expression between 5/6 nephrectomized and sham-operated mouse was measured on the brain.