Expression data from the kidney tissue of Han:SPRD rats
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE75578 | GEO | 2015/12/02
SECONDARY ACCESSION(S): PRJNA304622
REPOSITORIES: GEO
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Project description:Han:SPRD Cy is a spontaneous rat model of polycystic kidney disease (PKD) caused by a missense mutation in Pkdr1. Cystogenesis in this model is not clearly understood. In the current study, we performed global gene expression profiling in early-stage PKD cyst development in Cy/Cy kidneys and normal (+/+) kidneys, at 3 and 7 days of postnatal age. Expression profiles were determined by microarray analysis, followed by validation with real-time RT-PCR. Genes were selected with over 1.5 fold expression changes compared with age-matched +/+ kidneys for canonical pathway analysis. We found 9 pathways in common between 3-day and 7-day Cy/Cy kidneys. Three significantly changed pathways were designated 'VDR/RXR Activation,' 'LPS/IL-1 Mediated Inhibition of RXR Function,' and 'LXR/RXR Activation'. These results suggest that RXR mediated signaling is significantly altered in developing kidneys with mutated Pkdr1. In gene ontology analysis, the functions of these RXR-related genes were found to be involved in regulating cell proliferation and organ morphogenesis. With real-time RT-PCR analysis, the up-regulation of Ptx2, Alox15b, OSP and PCNA, major markers of cell proliferation associated with the RXR pathway, were confirmed in 3- and 7-day Cy/Cy kidneys compared with 3-day +/+ kidneys. The increased RXR protein was observed both in nuclei and cytoplasm of cystic epithelial cells in early-stage Cy/Cy kidneys, and the RXR-positive cells were strongly positive for PCNA staining. Taken together, cell proliferation and organ morphogenesis signals transduced by RXR mediated pathways may have important roles for cystogenesis in early-stage PKD in this Pkdr1-mutated Cy rat.
2011-12-09 | GSE23079 | GEO
Project description:Background: Autosomal dominant polycystic kidney disease (ADPKD) affects more than 12 million people worldwide. Mutations in PKD1 and PKD2 cause cyst formation through unknown mechanisms. To unravel the pathogenic mechanisms in ADPKD, multiple studies have investigated transcriptional mis-regulation in cystic kidneys from patients and mouse models, and numerous dysregulated genes and pathways have been described. Yet, the concordance between studies has been rather limited. Furthermore, the cellular and genetic diversity in cystic kidneys has hampered the identification of mis-expressed genes in kidney epithelial cells with homozygous PKD mutations, which are critical to identify polycystin-dependent pathways. Methods: Autosomal dominant polycystic kidney disease (ADPKD) affects more than 12 million people worldwide. Mutations in PKD1 and PKD2 cause cyst formation through unknown mechanisms. To unravel the pathogenic mechanisms in ADPKD, multiple studies have investigated transcriptional mis-regulation in cystic kidneys from patients and mouse models, and numerous dysregulated genes and pathways have been described. Yet, the concordance between studies has been rather limited. Furthermore, the cellular and genetic diversity in cystic kidneys has hampered the identification of mis-expressed genes in kidney epithelial cells with homozygous PKD mutations, which are critical to identify polycystin-dependent pathways. Results: Autosomal dominant polycystic kidney disease (ADPKD) affects more than 12 million people worldwide. Mutations in PKD1 and PKD2 cause cyst formation through unknown mechanisms. To unravel the pathogenic mechanisms in ADPKD, multiple studies have investigated transcriptional mis-regulation in cystic kidneys from patients and mouse models, and numerous dysregulated genes and pathways have been described. Yet, the concordance between studies has been rather limited. Furthermore, the cellular and genetic diversity in cystic kidneys has hampered the identification of mis-expressed genes in kidney epithelial cells with homozygous PKD mutations, which are critical to identify polycystin-dependent pathways. Conclusions: Autosomal dominant polycystic kidney disease (ADPKD) affects more than 12 million people worldwide. Mutations in PKD1 and PKD2 cause cyst formation through unknown mechanisms. To unravel the pathogenic mechanisms in ADPKD, multiple studies have investigated transcriptional mis-regulation in cystic kidneys from patients and mouse models, and numerous dysregulated genes and pathways have been described. Yet, the concordance between studies has been rather limited. Furthermore, the cellular and genetic diversity in cystic kidneys has hampered the identification of mis-expressed genes in kidney epithelial cells with homozygous PKD mutations, which are critical to identify polycystin-dependent pathways.
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Project description:Gender has strong impact on kidney performance. Female gender tends to be renal protective. PKD/Mhm is rat model for human polycystic kidney disease (PKD) caused by a mutation in gene Anks6. PKD progresses faster in male rats compared with females. We used microarrays to detect gender-dependent gene expression in kidney of 36d old PKD/Mhm rats. Experiment Overall Design: Gender-dependent gene expression was examined both in heterozygous PKD/Mhm rats affected with PKD and in their wild type littermates. Three microarrays were hybridized for each combination of gender and genotype.
2009-10-11 | E-GEOD-13065 | biostudies-arrayexpress
Project description:Gender has strong impact on kidney performance. Female gender tends to be renal protective. PKD/Mhm is rat model for human polycystic kidney disease (PKD) caused by a mutation in gene Anks6. PKD progresses faster in male rats compared with females. We used microarrays to detect gender-dependent gene expression in kidney of 36d old PKD/Mhm rats. Keywords: gender, genotype
2009-09-30 | GSE13065 | GEO
Project description:Plant inflorescence meristems and floral meristems possess specific boundary domains that result in floral organ separation, and in proper numbers of floral organs. HANABA TARANU (HAN) encodes a boundary-expressing GATA type zinc finger transcription factor that regulates shoot apical meristem organization, cell division and flower development in Arabidopsis, but the underlying mechanism remains unclear. Through time-course whole genome oligonucleotide microarray analyses following transient overexpression of HAN, we find that HAN represses hundreds of genes, especially genes involved in hormone responses and floral organ regulation. Transient overexpression of HAN also causes the repression of HAN itself and three other HAN family genes: HANL2 (HAN-LIKE2), GNC (GATA, NITRATE-INDUCIBLE, CARBON-METABOLISM-INVOLVED) and GNL (GNC LIKE), forming a negative regulatory feedback loop. Double- and triple-mutant strains of han with hanl2, gnc and gnl show synergistic effects on sepal fusion, petal number, and silique length, and embryo development, as well as carpelloid stamens. Transcripts of HANL2, GNC and GNL have similar accumulation patterns, specifically in petals, stamens, carpels and inflorescence meristems, which are partially overlapping with the expression pattern of HAN, suggesting that HAN and HAN family genes share redundant functions during flower development. We further show by yeast two hybrid assays that HAN can homodimerize as well as heterodimerize with other HAN family proteins. Chromatin-immunoprecipitation analyses indicate that HAN directly binds to its own promoter and the promoter of GNC in vivo. These findings, together with the fact that constitutive overexpression of HAN has an even stronger phenotype than a loss of function mutation, support the hypothesis that HAN may function as a key repressor that regulates floral development via intricate regulatory networks involving genes in the GATA3 family, hormone actions and floral organ specification.
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2015-07-23 | GSE71226 | GEO
Project description:The genetics, social, cultural and environmental factors pose a great challenge for the diagnosis and treatment of coronary heart disease among different racial groups. We aimed to identify the differentially expressed genes involved in coronary heart disease in Chinese Han people as an aid for screening and diagnosing coronary heart disease. We used microarrays to detail the global programme of gene expression to identify the differentially gene between the patients with coronary heart disease and healthy people in Chinese Han people Three patients with coronary heart disease and three healthy people in Chinese Han people were recruited,total RNA of each samples were extracted from peripheral blood to hybridize with Affymetrix microarrays.
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