Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Identification of renal distal convoluted tubules enriched genes

ABSTRACT: The renal distal convoluted tubule DCT is a short part of the distal nephron with specific functions transporting ions and thereby modifying Na, Ca, Mg, K balance A transcriptomic analysis of the DCT was performed to identify specific gene expression which would implicate those genes in specific DCT function Fluorescent DCT (EGFP+) were sorted out from a renal tubule suspension by a COPAS (Complex Object Parametric analyser and sorter). EGFP- and the total (ALL) fractions were also sorted by COPAS. Gene expression for each fractions (EGFP+, EGFP-, ALL) was performed in 4 mice

ORGANISM(S): Mus musculus

SUBMITTER: Nicolas Picard

PROVIDER: E-GEOD-51935 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Protein phosphatase 1 inhibitor-1 deficiency reduces phosphorylation of renal NaCl cotransporter and causes arterial hypotension.

Picard Nicolas N Trompf Katja K Yang Chao-Ling CL Miller R Lance RL Carrel Monique M Loffing-Cueni Dominique D Fenton Robert A RA Ellison David H DH Loffing Johannes J

Journal of the American Society of Nephrology : JASN 20131114 3

The thiazide-sensitive NaCl cotransporter (NCC) of the renal distal convoluted tubule (DCT) controls ion homeostasis and arterial BP. Loss-of-function mutations of NCC cause renal salt wasting with arterial hypotension (Gitelman syndrome). Conversely, mutations in the NCC-regulating WNK kinases or kelch-like 3 protein cause familial hyperkalemic hypertension. Here, we performed automated sorting of mouse DCTs and microarray analysis for comprehensive identification of novel DCT-enriched gene pro ...[more]

PMID: 24231659

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Project description:Renal excretion of water and major electrolytes exhibits a significant circadian rhythm. This functional periodicity is believed to result, at least in part, from circadian changes in secretion/reabsorption capacities of the distal nephron and collecting ducts. Here, we studied the molecular mechanisms underlying circadian rhythms in the distal nephron segments, i.e. distal convoluted tubule (DCT) and connecting tubule (CNT) and, the cortical collecting duct (CCD). Temporal expression analysis performed on microdissected mouse DCT/CNT or CCD revealed a marked circadian rhythmicity in the expression of a large number of genes crucially involved in various homeostatic functions of the kidney. This analysis also revealed that both DCT/CNT and CCD possess an intrinsic circadian timing system characterized by robust oscillations in the expression of circadian core clock genes (clock, bma11, npas2, per, cry, nr1d1) and clock-controlled Par bZip transcriptional factors dbp, hlf and tef. The clock knockout mice or mice devoid of dbp/hlf/tef (triple knockout) exhibit significant changes in renal expression of several key regulators of water or sodium balance (vasopressin V2 receptor, aquaporin-2, aquaporin-4, M-oM-^AM-!ENaC). Functionally, the loss of clock leads to a complex phenotype characterized by partial diabetes insipidus, dysregulation of sodium excretion rhythms and a significant decrease in blood pressure. Collectively, this study uncovers a major role of molecular clock in renal function. Experiment Overall Design: We examined the temporal profiles of gene expression in mouse distal nephron segments and collecting ducts. The RNA was extracted from microdissected distal convoluted tubules and connecting tubules (DCT/CNT samples) or, cortical collecting ducts (CCD samples). Animals were sacrificed for microdissection every 4 hours, i.e. at ZT0, ZT4, ZT8, ZT12, ZT16 and ZT20 (ZT M-bM-^@M-^S Zeitgeber (circadian) time, indicates time of light-on as ZT0 and time of light-off as ZT12). The microarray hybridization was performed in duplicates on two pools of RNA composed of equivalent amounts of RNA prepared from five animals at each ZT time-point.

Dataset Information

Identification of renal distal convoluted tubules enriched genes

Publications

Protein phosphatase 1 inhibitor-1 deficiency reduces phosphorylation of renal NaCl cotransporter and causes arterial hypotension.

Similar Datasets

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