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E-GEOD-7257

ABSTRACT: Transcription profiling of mouse wild type and Lim1-null renal vesicles microdissected from embryonic day 12.5 kidneys

OTHER RELATED OMICS DATASETS IN: PRJNA98013

PROVIDER: E-GEOD-7257 | ExpressionAtlas | 2014-07-08

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-GEOD-7257-analysis-methods.tsv	Tabular
	E-GEOD-7257-atlasExperimentSummary.Rdata	Rdata
	E-GEOD-7257-configuration.xml	Xml
	E-GEOD-7257-percentile-ranks.tsv	Tabular
	E-GEOD-7257.condensed-sdrf.tsv	Tabular

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Gestational high salt stressed Embryonic Day 14.5 BdkrB2 Null Mouse Kidney vs. BdkrB2 Wild Type Mouse Kidney

Project description:Transcriptional profiling of Embryonic Day 14.5 mouse kidneys comparing the infuence of gestational high salt stress on gene expression remolding of BdkrB2 receptor null mice with that of BdkrB2 receptor wild type mice. The BdkrB2 receptor has been shown to be playing a role in renal vascular tone, kidney secretion and reabsorption function, normal kidney development, while impaired BdkrB2 receptor in kidney shown being associated with renal agenesis and renal dysplasia. Goal was to determine the effects of BdkrB2 receptor knockout together with gestational high salt stress on renal gene expression pattern.

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Gestational high salt stressed Embryonic Day 14.5 BdkrB2 Null Mouse Kidney vs. BdkrB2 Wild Type Mouse Kidney

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Project description:Autosomal dominant polycystic kidney disease (ADPKD) is characterized by cyst formation throughout the kidney parenchyma. It is caused by mutations in either of two genes, PKD1 and PKD2. Mice that lack functional Pkd1 (Pkd1null/null), develop rapidly progressive cystic disease during embryogenesis, and serve as a model to study human ADPKD. We examined the molecular pathways that modulate renal cyst growth in the Pkd1null/null model by performing global gene-expression proﬁling in embryonic kidneys at day 14 and 17. Gene Ontology and gene set enrichment analysis were used to identify overrepresented signaling pathways in Pkd1null/null kidneys. We found dysregulation of developmental, metabolic, and signaling pathways (e.g. Wnt, calcium, TGF-b and MAPK) in Pkd1null/null kidneys. Total RNA were obtained from kidneys of wild-type and Pkd1null/null animals at embryonic ages 14.5 and 17.5.

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Transcription profiling of mouse wild type and Lim1-null renal vesicles microdissected from embryonic day 12.5 kidneys

Project description:The Lim1 gene has essential functions during several stages of kidney development. In particular, a tissue specific knockout in the early metanephric mesenchyme results in the formation of the earliest nephron precursor, the renal vesicle, but failure of this structure to progress to the next stage, the comma shaped body. To better understand the molecular nature of this developmental arrest we used a laser capture microdissection-microarray strategy to examine the perturbed gene expression pattern of the mutant renal vesicles. Among the genes found differently expressed were Chrdl2, an inhibitor of BMP signaling, the pro-apoptotic factor Bmf, as well as myob5, an atypical myosin which modulates chemokine and transferring signaling, and pdgfr1, which is important in epithelial folding. Of particular interest, the microarray data indicated that the Dkk1 gene, which encodes an inhibitor of Wnt signaling, was downregulated nine fold in mutants. This was confirmed by in situ hybridizations. It is interesting to note that Lim1 and Dkk1 mutant mice have striking similarities in phenotype. These results suggest that the Dkk1 gene might be a key downstream effector of Lim1 function. Experiment Overall Design: We compared gene expression profiles of wild type and mutant Lim1 renal vesicles, which were isolated from E12.5 kidneys by laser capture microdissection. Nine biological independent samples were examined, with four mutant and five wild type. Each sample included approximately 30-50 renal vesicles. Detailed protocols are described at GUDMAP.org

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