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PROVIDER: PRJNA259967 | ENA |
REPOSITORIES: ENA
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Project description:Alteration of mRNA and microRNA expression profiles in rat muscular type vasculature in early postnatal development [mRNA]
| PRJNA259969 | ENA
Project description:Alteration of mRNA and microRNA expression profiles in rat muscular type vasculature in early postnatal development [miRNA]
| PRJNA259970 | ENA
Project description:This study tested the hypothesis that mRNA expression profiles change in the muscular type rat saphenous artery during early postnatal development. To explore this, we performed mRNA microarray analysis on muscular type saphenous arteries of young (10-12 days) and adult (2-3 months) rats.
2015-04-30 | GSE60961 | GEO
Project description:This study tested the hypothesis that mRNA expression profiles change in the muscular type rat saphenous artery during early postnatal development. To explore this, we performed mRNA microarray analysis on muscular type saphenous arteries of young (10-12 days) and adult (2-3 months) rats. For one sample four saphenous arteries from 2 young animals (n = 4 samples per group) or two saphenous arteries from one adult animal (n = 4 samples per group) were used to profile mRNA (n = 8; GeneChip® Rat Gene 1.0) expression changes during the muscular type rat saphenous artery during early postnatal development. In this study, 10-12 days old (“young”) and 2 - 3 months old (“adult”) male Wistar rats.
2015-04-30 | E-GEOD-60961 | biostudies-arrayexpress
Project description:This study tested the hypothesis that miRNA expression profiles change in the muscular type rat saphenous artery during early postnatal development. To explore this, we performed miRNA microarray analysis on muscular type saphenous arteries of young (10-12 days) and adult (2-3 months) rats.
2015-04-30 | GSE60962 | GEO
Project description:This study tested the hypothesis that miRNA expression profiles change in the muscular type rat saphenous artery during early postnatal development. To explore this, we performed miRNA microarray analysis on muscular type saphenous arteries of young (10-12 days) and adult (2-3 months) rats. For one sample four saphenous arteries from 2 young animals (n = 4 samples per group) or two saphenous arteries from one adult animal (n = 4 samples per group) were used to profile miRNA (n = 8; GeneChip® miRNA 3.0) expression changes during the muscular type rat saphenous artery during early postnatal development. In this study, 10-12 days old (“young”) and 2 - 3 months old (“adult”) male Wistar rats were used.
2015-04-30 | E-GEOD-60962 | biostudies-arrayexpress
Project description:mRNA profiles of livers during postnatal development
| PRJNA944575 | ENA
Project description:Rationale: The Id1 and Id3 genes play major roles during cardiac development, despite their expression being confined to non-myocardial layers (endocardium â?? endothelium - epicardium). We previously described that Id1â??/â??Id3â??/â?? double knockout (dKO) mouse embryos die at mid-gestation from multiple cardiac defects, but early demise precluded the studies of the roles of Id in the adult mice. Objective: To elucidate postnatal roles of Id genes in the heart. Methods and Results: We ablated Id1 gene in the vasculature and Id3 gene globally to generate Tie2Cre+Id1F/â??Id3â??/â?? and Tie2Cre+Id1F/FId3â??/â?? conditional KO (Id cKO) embryos. Half of the Id cKO mice die at birth. Postnatal demise was associated with cardiac underdevelopment, enlargement, muscular ventricular septal and endothelial defects. Surviving Id cKO mice exhibited dilated, fibrotic cardiomyopathy associated with defects in the vasculature. The adult cardiac phenotype progressed into heart failure and resembled endomyocardial fibroelastosis. An abnormal vascular response was also observed in the healing process of excisional skin wounds of Id cKO mice. Expression patterns of vascular, fibrotic and hypertrophic markers were altered in the Id cKO hearts, but addition of Insulin-Like Growth Factor binding protein-3 (IGFbp3) reversed gene expression profiles of vascular and fibrotic, but not hypertrophic markers. Conclusions: Conditional ablation of Id genes in the vasculature leads to dilated fibrotic cardiomyopathy. The findings could reveal important insights into the role(s) of the endocardial network of the endothelial lineage to the development of dilated fibrotic cardiomyopathy and identify a potential therapeutic target, IGFbp3, in its treatment. Total RNA from heart tissue was isolated (RNeasy, QIAGEN) from P180 WT, Id control, Id cKO, IGFbp3 incubated Id cKO, and control incubated Id cKO. RNA was converted to cDNA, cRNA, and hybridized to DNA sequences contained in the GeneChip Mouse Gene 1.0 ST Array (Affymetrix). Information from at least duplicate samples was compared and filtered by fold change >2 (Id cKO vs WT, Id control vs WT, IGFbp3 incubated Id cKO vs. control incubated Id cKO) and statistical p-value<0.001.
2010-10-07 | E-GEOD-21924 | biostudies-arrayexpress
Project description:To unravel the gene expression changes during postnatal prefrontal cortex development, RNA-seq was performed in the rat medial prefrontal cortex at five time points from early life to adulthood (postnatal day 8, 14, 21, 35 and 70) and differential expression of protein-coding genes, lincRNAs and alternative exons was analyzed. A switch from neuronal network development to maintenance during postnatal rat prefrontal cortex development was shown.
2017-01-01 | GSE79860 | GEO
Project description:Rationale: The Id1 and Id3 genes play major roles during cardiac development, despite their expression being confined to non-myocardial layers (endocardium – endothelium - epicardium). We previously described that Id1–/–Id3–/– double knockout (dKO) mouse embryos die at mid-gestation from multiple cardiac defects, but early demise precluded the studies of the roles of Id in the adult mice. Objective: To elucidate postnatal roles of Id genes in the heart. Methods and Results: We ablated Id1 gene in the vasculature and Id3 gene globally to generate Tie2Cre+Id1F/–Id3–/– and Tie2Cre+Id1F/FId3–/– conditional KO (Id cKO) embryos. Half of the Id cKO mice die at birth. Postnatal demise was associated with cardiac underdevelopment, enlargement, muscular ventricular septal and endothelial defects. Surviving Id cKO mice exhibited dilated, fibrotic cardiomyopathy associated with defects in the vasculature. The adult cardiac phenotype progressed into heart failure and resembled endomyocardial fibroelastosis. An abnormal vascular response was also observed in the healing process of excisional skin wounds of Id cKO mice. Expression patterns of vascular, fibrotic and hypertrophic markers were altered in the Id cKO hearts, but addition of Insulin-Like Growth Factor binding protein-3 (IGFbp3) reversed gene expression profiles of vascular and fibrotic, but not hypertrophic markers. Conclusions: Conditional ablation of Id genes in the vasculature leads to dilated fibrotic cardiomyopathy. The findings could reveal important insights into the role(s) of the endocardial network of the endothelial lineage to the development of dilated fibrotic cardiomyopathy and identify a potential therapeutic target, IGFbp3, in its treatment.
2010-10-07 | GSE21924 | GEO