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5/6 nephrectomy (5/6Nx) effect on the brain

ABSTRACT: 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-β1 expression from the kidney. Abnormal TGF-β 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-β signal.

ORGANISM(S): Mus musculus

PROVIDER: GSE35134 | GEO | 2013/08/01

SECONDARY ACCESSION(S): PRJNA155991

REPOSITORIES: GEO

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5/6 nephrectomy (5/6Nx) effect on the brain

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.

2013-08-01 | E-GEOD-35134 | biostudies-arrayexpress

Influence of retinol on kidney in 5/6 nephrectomy mice

Project description:The circadian clock has been found to be associated with various diseases. We showed that 5/6 nephrectomy (5/6Nx) Clk/Clk mice, which show mutation in the gene encoding circadian locomotor output cycles (Clock) do not show aggravation of renal fibrosis because transforming growth factor-1 (Tgf-1) expression is not increased. In wild-type 5/6Nx kidneys, we found that retinoid, a metabolite of retinol, led to alteration of the expresion 24-h rhythm of Clock expression. Renal Tgf- 1 expression is activated by Clock and further aggravates renal dysfunction by causing fibrosis. We also showed that, in 5/6Nx mice fed a retinol-free diet, renal fibrosis and apoptosis are reduced, leading to a marked improvement in serum creatinine levels. Moreover, our study identified hepatic Cyp3a11 and Cyp26a1 as key retinol metabolism-related genes whose expression decreased in 5/6Nx mice. Our data indicated that the negative chain reaction of metabolic clock alteration in between the kidney and liver aggravates renal dysfunction.

2014-06-06 | GSE57799 | GEO

Circadian rhythm in clock mutants

Project description:Circadian rhythm in clock mutants

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Control of bladder peripheral clock and diurnal micturition pattern by glucocorticoids

Project description:Peripheral clocks function to regulate each organ and are synchronized though various molecular and behavioral signals. However, signals that entrain the bladder clock remain elusive. Here, we show that glucocorticoids are a key cue for the bladder clock in vitro and in vivo. A pBmal1-dLuc human urothelial cell line showed significant shifts in gene expression after cortisol treatment while, in vivo, rhythmic bladder clock gene expression was not influenced by bilateral-adrenalectomy (ADx) but shifted 4 hours forward by corticosterone administration at the inactive phase (CORT). Moreover, the bladder clock shifted 8-12 hours in ADx+CORT mice. These mice saw decreases in the diurnal rhythm of volume voided per micturition, while maintaining diurnal activity rhythm. These results indicate that the diurnal rhythm of glucocorticoid signaling is a zeitgeber that overcomes other entrainment factors for the bladder clock and coordinates the diurnal rhythm of volume voided per micturition. (145 words)

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Hepatic transcriptome by Next Generation Sequencing of WT and clock mutant mice fed a HFD ad libitum or time-restricted feeding.

Project description:Increased susceptibility of circadian clock mutant mice to metabolic diseases has led to the understanding that a molecular circadian clock is necessary for metabolic homeostasis. Circadian clock produces a daily rhythm in activity-rest and an associated rhythm in feeding-fasting. Feeding-fasting driven programs and cell autonomous circadian oscillator act synergistically in the liver to orchestrate daily rhythm in metabolism. However, an imposed feeding-fasting rhythm, as in time-restricted feeding, can drive some rhythm in liver gene expression in clock mutant mice. We tested if TRF alone, in the absence of a circadian clock in the liver or in the whole animal can prevent obesity and metabolic syndrome. Mice lacking the clock component Bmal1 in the liver, Rev-erb alpha/beta in the liver or cry1-/-;cry2-/- (CDKO) mice rapidly gain weight and show genotype specific increased susceptibility to dyslipidemia, hypercholesterolemia and glucose intolerance under ad lib fed condition. However, when the mice were fed the same diet under time-restricted feeding regimen that imposed 10 h feeding during the night, they were protected from weight gain and other metabolic diseases. Transcriptome and metabolome analyses of the liver from there mutant mice showed TRF reduces de novo lipogenesis, increased beta-oxidation independent of a circadian clock. TRF also enhanced cellular defense to metabolic stress. These results suggest a major function of the circadian clock in metabolic homeostasis is to sustain a daily rhythm in feeding and fasting. The feeding-fasting cycle orchestrates a balance between nutrient stress and cellular response to maintain homeostasis.

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Circadian rhythm in Clock mutant and Cry deficient mice

Project description:Molecular analysis of circadian rhythm in mice. Liver tissue of wildtype, Clock mutant and Cry deficient C57BL/6 8- to 10-week-old male mice examined. Keywords = circadian rhythm Keywords: other

2003-11-08 | GSE454 | GEO

Human mesenchymal stem cells prevent neurological complications of radiotherapy

Project description:Human mesenchymal stem cells prevent neurological complications of radiotherapy

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5/6 nephrectomy (5/6Nx) effect on the liver

Project description:Chronic renal failure (CRF) is associated with a decrease in drug metabolism. The present study investigated the repercussions of CRF on liver cytochrome P450 (CYPs), but the mechanisms have been little explored. On the other hand, the expression of several CYP genes exhibits circadian rhythm. Here we report that downregulation of hepatic CYP3A11 (the murine homolog to human CYP3A4; the most decrease in 5/6Nx using microarray analysis) by suppressing the expression of clock gene; D-site binding protein (DBP). In vivo experiments, the mRNA levels of hepatic CYP3A11 exhibit circadian rhythm regulated by DBP and E4BP4, and significantly decreased in 5/6Nx. Microarray analysis revealed that the general transcription factors of CYP3A11 did not changed. However, DBP were downregulated and several CYP genes controlled by DBP also significantly decreased in 5/6Nx. These downregulations were not observed in angiotensin II type 1alpha receptor (AT II R1a) deficient 5/6Nx because serum TGF-betaM-BM- was not upregulate. In vitro experiments, the RNA levels of CYP3A11 and DBP were downregulated in wild-type mouse hepatocytes incubated with serum from 5/6Nx, but did not changed in Id2 (-/-) hepatocytes. In fact, hepatic Id2 was upregulated and caused the downregulation of DBP in 5/6Nx. Hepatocyte treated with SD208 (TGF-beta receptor 1 selectivity inhibitor) recovered CYP3A11, DBP and Id2 to control levels. Furthermore, 5/6Nx treated with tranilast (inhibitor of TGF-beta production or isolation) or candesartan (ARBs) also recovered CYP3A11 levels. Our findings define that DBP has effects on downregulation of CYP3A11. In CRF conditions, TGF-beta is upregulated by angiotensin II receptor in renal and downregulates DBP and CYP3A11 levels mediated by Id2 in liver. Furthermore, downregulation of CYP3A11 can prevent by tranilast or candesartan. Differential gene expression between 5/6 nephrectomized and sham-operated mouse was measured on the liver.

2013-08-01 | E-GEOD-35135 | biostudies-arrayexpress

Comparison study between Uremic patient with Healthy control

Project description:Patients with chronic kidney disease (CKD) have significantly increased morbidity and mortality resulting from infections and cardiovascular diseases. Since monocytes play an essential role in host immunity, this study was directed to explore the gene expression profile and to identify differences in activated pathways in monocytes relevant to the pathophysiology of atherosclerosis and increased susceptibility to infections. Monocytes from CKD patients (stages 4 and 5, eGFR <20 ml/min x 1.73 m2) and healthy donors were collected from peripheral blood. Microarray gene expression profile was done and data were interpreted by Genespring software and Panther tools website. Western blot was done to validate the pathway members. The results demonstrated that 487 and 258 genes were differentially up- and down regulated respectively in the patient group. Pathways involved in the inflammatory response were highly expressed and the Wnt/β- catenin signaling pathway was the most significant pathway expressed in the patient group (P=0.02). Since this pathway has been attributed to a variety of inflammatory manifestations, the current finding may contribute to dysfunctional monocytes in CKD patients. To develop strategies to interfere with this pathway may improve host immunity and prevent cardiovascular complications in CKD patients. Six gene expression Affymetrix chip were used. Three for each group

2013-01-15 | E-GEOD-43484 | biostudies-arrayexpress

Transcription profiling of livers from wild type, Clock mutant and Cry deficient C57BL/6 mice to characterize CLOCK-regulated circadian output genes.

Project description:Molecular analysis of circadian rhythm in mice. Liver tissue of wildtype, Clock mutant and Cry deficient C57BL/6 8- to 10-week-old male mice examined.

2007-11-07 | E-GEOD-454 | biostudies-arrayexpress

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