Rattus norvegicus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA389116 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Akap1 KO and Wt mice were exposed to normoxia or hyperoxia for 48h. Total RNA was extracted from lungs of Wt Normoxia (n=3), Wt hyperoxia (n=3), Akap1 KO (n=3) and Akap1 hyperoxia (n=3) mice. RNA-sequencing was carried out followed by differential expression of genes in the following groups. Wt Normoxia vs Wt Hyperoxia, Akap1 KO Normoxia versus Akap1 KO Hyperoxia, Wt Normoxia versus Akap1 KO Normoxia and Wt Hperoxia versus Akap1 Hyperoxia.
2022-10-26 | GSE173295 | GEO
Project description:miRNA profile of Neonatal Rat Cardiomyocytes treated with 0.5% or 1.5% Oxygen for 48 h versus Normoxia
| PRJNA131995 | ENA
Project description:Background: Bronchopulmonary dysplasia (BPD), the most common complication of extreme preterm birth, can be caused by oxygen-related lung injury and is characterized by impaired alveolar and vascular development. Mesenchymal stromal cells (MSCs) have lung protective effects. Conversely, BPD is associated with increased MSCs in tracheal aspirates. Objective: To determine whether endogenous lung (L-)MSCs are perturbed in a well-established oxygen-induced rat model mimicking BPD features. Methods: Rat pups were exposed to room air or 95% oxygen from birth to postnatal day 10. On day 12, CD146+ L-MSCs were isolated and characterized according to the International Society for Cellular Therapy criteria. Epithelial and vascular repair potential were tested by scratch assay and endothelial network formation respectively, immune function by mixed lymphocyte reaction assay. Microarray analysis was performed using the Affymetrix GeneChip and gene set enrichment analysis (GSEA) software. Results: CD146+ L-MSCs isolated from rat pups exposed to hyperoxia had decreased CD73 expression and inhibited lung endothelial network formation. CD146+ L-MSCs indiscriminately promoted epithelial wound healing and limited T-cell proliferation. Expression of potent anti-angiogenic genes of the axonal guidance cue and CDC42 pathways was increased after in vivo hyperoxia, whereas genes of the anti-inflammatory JAK/STAT and lung/vascular growth promoting Fibroblast Growth Factor (FGF) pathways were decreased. Conclusions: In vivo hyperoxia exposure alters the pro-angiogenic effects and FGF expression of L-MSCs. Additionally, decreased CD73 and JAK/STAT expression suggest decreased immune function. L-MSC function may be perturbed and contribute to BPD pathogenesis. These findings may lead to improvements in manufacturing exogenous MSCs with superior repair capabilities.
2017-06-03 | GSE99633 | GEO
Project description:Gene analysis of the neonatal rat lung exposed to STZ-induced maternal diabetes
| PRJNA111303 | ENA
Project description:We performed miRNA array analysis from 4 groups (neonatal lung control, neonatal lung after hyperoxia, adult lung control, adult lung after hyperoxia). We used pools of every 100ng of total RNA of three samples for each groups.
2015-07-15 | GSE70873 | GEO
Project description:In this study the microRNA expression of primary murine (C57BL/6) lung alveolar type II cells belonging to four different conditions was analyzed. Effects of hyperoxia 24 hours group were compared to the normoxia 24 hours and effects of the hyperoxia 6 hours group were compared to the normoxia 6 hours.
2017-12-16 | GSE92551 | GEO
Project description:Electric stimulation of neonatal rat ventricular cardiomyocytes
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Project description:In order to establish a rat embryonic stem cell transcriptome, mRNA from rESC cell line DAc8, the first male germline competent rat ESC line to be described and the first to be used to generate a knockout rat model was characterized using RNA sequencing (RNA-seq) analysis.
2016-09-02 | GSE44150 | GEO
Project description:miR154-3p and -5p are mainly expressed in the lung epithelium pre- and postnatally in mice and are significantly higher expressed upon hyperoxia (BPD mouse model). In normoxia in vivo overexpression of miR154 (CCSPrtTA;tetOmiR154, P0-P16) leads to increased Fgf10 signaling and Tgf- signaling. Furthermore, avleolar morphometry revealed increased MLI indicating interference with alveologenesis at P16. In hyperoxia (P0-P8) in vivo overexpression of miR154 (CCSPrtTA;tetOmiR154, P0-P16) leads to decreased Fgf10 signaling and Tgf- signaling.
2020-05-21 | GSE141267 | GEO