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Gene expression in rat kidney following recovery from acute renal failure (ARF)

ABSTRACT: This experiment was designed to study the alteration in expression of mRNA is kidney following recovery from transient acute renal failure. The model used was a 52 min. bilateral renal artery clamping, followed by reperfusion, which resulted in a transient loss of renal function, followed by a functional recovery. All tissue in this study was harvested 35 days post-surgery, when renal function was restored, and renal structure largelyy normal. For controls, sham-operated animals were used. An N of 6 post-ischemia reperfusion animals were used with 6 sham-operated controls. For hybridization studies, RNA from one of six post-ischemic acute renal failure animals were compared with with RNA from kidney of six sham-operated control animals. Each ARF vs. sham-operated comparison was performed twice, alternating the cy3 and cy5 label between the two hybridizations for each pair. A second set of hybridizations was carried out using sham vs. sham hybridizations. This was done to get a quantitative analysis of the variation of the biological and microarry platform. Keywords: parallel sample

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE1714 | GEO | 2005/01/26

SECONDARY ACCESSION(S): PRJNA90373

REPOSITORIES: GEO

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Gene expression in rat kidney following recovery from acute renal failure (ARF)

Project description:This experiment was designed to study the alteration in expression of mRNA is kidney following recovery from transient acute renal failure. The model used was a 52 min. bilateral renal artery clamping, followed by reperfusion, which resulted in a transient loss of renal function, followed by a functional recovery. All tissue in this study was harvested 35 days post-surgery, when renal function was restored, and renal structure largelyy normal. For controls, sham-operated animals were used. An N of 6 post-ischemia reperfusion animals were used with 6 sham-operated controls. For hybridization studies, RNA from one of six post-ischemic acute renal failure animals were compared with with RNA from kidney of six sham-operated control animals. Each ARF vs. sham-operated comparison was performed twice, alternating the cy3 and cy5 label between the two hybridizations for each pair. A second set of hybridizations was carried out using sham vs. sham hybridizations. This was done to get a quantitative analysis of the variation of the biological and microarry platform.

2010-06-10 | E-GEOD-1714 | biostudies-arrayexpress

The role of Clec4e (Mincle) in microglia response to transient ischemic injury

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2016-03-24 | E-GEOD-77986 | biostudies-arrayexpress

Expression data from uninephrectomized dogs compared to sham operated dogs

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Project description:Lung ischemia-reperfusion (I/R) injury remains one of the common complications after various cardiopulmonary surgeries. I-R injury represents one potentially maladaptive response of the innate immune system which is featured by an exacerbated sterile inflammatory response triggered by tissue damage. Thus, understanding the key components and processes involved in sterile inflammation during lung I-R injury is critical to alter care and extend survival for patients with acute lung injury. We constructed a minipig surgical model of transient unilateral left pulmonary artery occlusion without bronchial involvement to create ventilated lung I-R injury. Lung tissues from minipig with sham operation (one sample), left side lung tissues (the operated side)(one sample) and right side lung tissues (the non-operated side)(one sample) from minipig with lung ischemia-reperfusion were submitted for gene expression array analysis.

2015-12-07 | E-GEOD-75560 | biostudies-arrayexpress

CaM Kinase II mediates maladaptive post-infarct remodeling but not acute myocardial ischemia/reperfusion injury

Project description:Calcium/calmodulin-dependent protein kinase II (CaMKII) was suggested to mediate ischemic myocardial injury and adverse cardiac remodeling. However, the specific functions of the CaMKII isoforms and splice variants in ischemia/reperfusion (I/R) injury have not been investigated yet. Thus, we studied the roles of the CaMKII isoforms and splice variants in I/R by the use of various CaMKII mutant mice. CaMKIIÎ´C was up-regulated already one day after I/R injury but surprisingly, acute I/R injury was neither affected in CaMKIIÎ´-deficient mice, CaMKIIÎ´-deficient mice in which the splice variants CaMKIIÎ´B and C were re-expressed nor in conditional CaMKIIÎ´/Î³ double-knockout mice (DKO). In contrast, 5 weeks after I/R, DKO mice were protected against extensive scar formation and cardiac dysfunction. Leukocyte infiltration was not altered one day but five days after I/R, explaining the late effects of CaMKII deletion on post-I/R remodeling. Other than reported before, we demonstrate that CaMKII is not critically involved in the immediate mechanisms that regulate acute I/R injury but in the process of post-infarct remodeling. We analysed 6 groups in total: 3 groups from wild-type control animals and 3 groups from CaMKII delta/gamma double-KO mice. Sham operated animals served as controls in both wild-type and KO animal groups. 2 different time points in ischia/reperfusion operated animals were investigated: 1 day and 5 days post-surgery.

2014-09-08 | E-GEOD-58486 | biostudies-arrayexpress

Transcriptional profiling of left ventricle and peripheral blood cells in rats with post-myocardial infarction

Project description:Myocardial infarction (MI) often results in left ventricular (LV) remodeling followed by heart failure (HF). It is of great clinical importance to understand the molecular mechanisms that trigger transition from compensated LV injury to HF and to identify relevant diagnostic biomarkers. In this study, we performed transcriptional profiling of LVs in rats with a wide range of experimentally induced infarct sizes and of peripheral blood mononuclear cells (PBMCs) in animals that developed HF. We used microarrays to investigate gene expression in the left ventricle (LV) accompanying myocardial infarction and concomitant heart failure (HF) in a well validated model of post-infarcted heart failure and to evaluate their reflection in peripheral blood mononuclear cells (PBMCs) Myocardial infarction (MI) was induced in male Wistar rats by ligation of the proximal left coronary artery. The sham-operated group (control group) was subjected to the same protocol, except that the suture was not tied around the proximal left coronary artery. Sham-operated rats (n=6) and rats with small (n=6), moderate (n=6), and large (n=5) MI size were included into the experiment two months after the operation. Then, left ventricules and blood samples were obtained for RNA extraction and hybridization on Affymetrix microarrays. Microarrays were used to compare the LV and PBMCs transcriptomes of control and experimental animals. The development of heart failure was estimated by echocardiography and catheterization.

2013-11-15 | E-GEOD-47495 | biostudies-arrayexpress

Expression data from murine cardiac fibroblasts and endothelial cells following Transverse Aortic Constriction

Project description:Accumulation of activated cardiac fibroblasts plays a key role in heart failure progression. These cells deposit excessive extracellular matrix that leads to mechanical stiffness, myocyte uncoupling and ischemia. To investigate whether two developmentally distinct cardiac fibroblast populations exhibit distinct expression profiles in response to cardiac injury, and therefore might necessitate distinct therapeutic targeting, we performed microarray analysis on FACS sorted cells. Tie2cre lineage traced CFs, non Tie2cre lineage traced cardiac fibroblasts and endothelial cells were isolated from left ventricle of SHAM operated and banded hearts at the onset of fibrosis, one week after surgery. We used microarrays to detail the global programme of gene expression in cardiac fibroblasts and endothelium following pressure overload. Tie2cre lineage traced, non-tie2cre lineage traced fibroblasts and endothelial cells were sorted from left ventricle of 3 SHAM operated and 3 TAC operated adult male Black Swiss mice. Tie2cre lineage traced, non-tie2cre lineage traced fibroblasts and endothelial cells were sorted from left ventricle of 3 SHAM operated and 3 Transaortic Constriction (TAC) operated adult male Black Swiss mice for RNA extraction and Affymetrix microarray analysis. Hypertrophy in TAC animals, an lack of hypertrophy in SHAM operated animals, was evaluated by hemodynamic measurements before surgery and one week after surgery. Cells were isolated one week after surgery.

2014-05-19 | E-GEOD-45820 | biostudies-arrayexpress

M2-like macrophages in the injured-kidney cortex promoted kidney cancer progression via the direct pro-tumor effect and the inhibition of CD8 T cell infiltration

Project description:In this study, we aimed to evaluate the effect of M2-like macrophages in the injured kidney on kidney cancer progression. As an acute kidney injury to chronic kidney disease model, we used unilateral ischemia-reperfusion injury (uIRI). And we inoculated RenCa cells, which are murine kidney cancer cell line, into renal subcapsule 14 days after uIRI (uIRI-Can) and compared uIRI-Can to RenCa cells inoculated into sham-operated renal subcapsule (Sham-Can) 20 days after inoculation. To identify gene characteristics of M2-like macrophages that are commonly detected both in the uIRI kidney cortex and uIRI-Can, we sorted Ly6Clow macrophages from 4 groups, uIRI kidney cortex, sham kidney cortex, uIRI-Can, and Sham-Can, and conducted RNA-Seq. This study revealed the characteristic gene expression of M2-like macrophages which were commonly detected in the injured kidney cortex and kidney cancer progressed on the injured kidney. And this could be a future therapeutic target of macrophage-targeted therapy.

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