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Lung transcript expression profile after Gata5 gene deletion

ABSTRACT: Gata5 is a zinc finger transcription factor that is expressed in embryonic pulmonary mesenchyme and becomes upregulated in the lungs, gut, and bladder during postnatal development. We used microarray to comapre gene expression profiles of mouse lung between Gata5 knockout and wild type mice. We hope to identify the differentially expressed genes that affected by Gata5 gene deletion and their functional clusters or pathways. The goal of this study is to identify the differentially expressed genes that affected by Gata5 gene deletion and their functional clusters or pathways.

ORGANISM(S): Mus musculus

PROVIDER: GSE47425 | GEO | 2013/08/26

SECONDARY ACCESSION(S): PRJNA205544

REPOSITORIES: GEO

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Lung transcript expression profile after Gata5 gene deletion

Project description:Gata5 is a zinc finger transcription factor that is expressed in embryonic pulmonary mesenchyme and becomes upregulated in the lungs, gut, and bladder during postnatal development. We used microarray to comapre gene expression profiles of mouse lung between Gata5 knockout and wild type mice. We hope to identify the differentially expressed genes that affected by Gata5 gene deletion and their functional clusters or pathways. The goal of this study is to identify the differentially expressed genes that affected by Gata5 gene deletion and their functional clusters or pathways. Total RNA samples from three Gata5 KO and four wild type control mouse left lungs were extracted from the mouse lungs and profiled using Affymetrix GeneChip Mouse Genome 430 2.0 Array.

2013-08-26 | E-GEOD-47425 | biostudies-arrayexpress

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Project description:Despite its high prevalence and economic burden, the etiology of human hypertension remains incompletely understood. Here we identify the transcription factor Gata5, as a new gene involved in regulation of blood pressure (BP). GATA5 is expressed in microvascular endothelial cells (mEC) and its genetic inactivation in mice leads to hypertension, vascular endothelial dysfunction and renal inflammation. Aged Gata5-Null mice develop salt-sensitivity and target-organ damage reminiscent of the progression of human hypertension. Endothelial-specific inactivation of Gata5 increases BP and leads to vascular endothelial dysfunction, confirming the endothelial component of Gata5 inactivation-related hypertension. To directly assess the effect of loss of GATA5 on endothelial cells, we generated a stable GATA5 knockdown cell line (HDMEC-Gata5KO) by infecting human dermal microvascular endothelial cells with a lentiviral vector containing an anti-Gata5 shRNA followed by a transcriptomic analysis. The control cells were infected with a lentivirus containing an empty vector pLKO2.

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Project description:Lung transcript expression profile after Gata5 gene deletion

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tableNONMMUT140591.1 may serve as a ceRNA to regulate Gata5 in UT-B knockout-induced cardiac conduction block

Project description:Objective: We intended to explore the potential molecular mechanisms underlying cardiac conduction block inducted by UT-B deletion at the transcriptome level. Methods: The heart tissues were harvested from UT-B null mice and age-matched wild-type mice for lncRNA sequencing analysis. Based on the sequencing data, the differentially expressed mRNAs (DEMs) and lncRNAs (DELs) between UT-B knockout and control groups were identified, followed by function analysis and mRNA-lncRNA co-expression analysis. The miRNAs were predicted, and then the competing endogenous RNA (ceRNA) network was constructed. Results: UT-B deletion results in the aberrant expression of 588 lncRNAs and 194 mRNAs. These DEMs were significantly enriched in inflammation-related pathway. A lncRNA-mRNA co-expression network and a ceRNA network was constructed on the basis of the DEMs and DELs. C7 (complement C7)-NONMMUT137216.1 co-expression pair had the highest correlation coefficient in the co-expression network. NONMMUT140591.1 had the highest degree in ceRNA network and involved in ceRNA of NONMMUT140591.1-mmu-miR-298-5p-Gata5 (GATA binding protein 5). Conclusion: UT-B deletion may promote cardiac conduction block via inflammatory process. The ceRNA NONMMUT140591.1-mmu-miR-298-5p-Gata5 may be a potential molecular mechanism of UT-B knockout-induced cardiac conduction block.

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Transcription profiling of two human cellular models of erythroid differentiation: K562 erythroid-leukemia cells treated with 1uM arabinofuranosyl-cytosine (AraC), and CD34+ stem cells treated with 7U/ml erythropoietin

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