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MicroRNA expression data in human fetal lungs

ABSTRACT: Microarray data of human fetal lungs between 16-23 weeks of gestation. The results provide a general insight into the microRNA expression profile during the canalicular phase of lung development.

ORGANISM(S): Homo sapiens

PROVIDER: GSE58139 | GEO | 2015/11/26

SECONDARY ACCESSION(S): PRJNA251966

REPOSITORIES: GEO

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MicroRNA expression data in human fetal lungs

Project description:Microarray data of human fetal lungs between 16-23 weeks of gestation. The results provide a general insight into the microRNA expression profile during the canalicular phase of lung development. Lung tissue samples for microarray analysis were obtained through the University of Pittsburgh Health Sciences Tissue Bank through an approved IRB protocol and de-identified using an honest broker system. Total RNA was labeled with Cy3 and hybridized on Agilent 8X15K microRNA array (Agilent Technologies, Santa Clara, CA). After 20 hours hybridization, arrays were washed and scanned according to the manufacturerâs protocol.

2015-11-26 | E-GEOD-58139 | biostudies-arrayexpress

MicroRNA expression data in mouse fetal lungs

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MicroRNA expression data in mouse fetal lungs

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Transcriptomic data from cultured human fetal lung tip-derived organoids at different stages of lung development

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Targeted NKX2.1 DamID sequencing data from human fetal lung organoids recapitulating differential developmental features of human lung development

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Sexual dimorphism in the fetal cardiac response to maternal nutrient restriction

Project description:Poor maternal nutrition causes intrauterine growth restriction (IUGR); however, its effects on fetal cardiac development are unclear. We have developed a baboon model of moderate maternal undernutrition, leading to IUGR. We hypothesized that the IUGR affects fetal cardiac structure and metabolism. Six control pregnant baboons ate ad-libitum (CTRL)) or 70% CTRL from 0.16 of gestation (G). Fetuses were euthanized at C-section at 0.9G under general anesthesia. Male but not female IUGR fetuses showed left ventricular fibrosis inversely correlated with birth weight. Expression of extracellular matrix protein TSP-1 was increased (p<0.05) in male IUGR. Expression of cardiac fibrotic markers TGFß, SMAD3 and ALK-1 were downregulated in male IUGRs with no difference in females. Autophagy was present in male IUGR evidenced by upregulation of ATG7 expression and lipidation LC3B. Global miRNA expression profiling revealed 56 annotated and novel cardiac miRNAs exclusively dysregulated in female IUGR, and 38 cardiac miRNAs were exclusively dysregulated in males (p<0.05). Fifteen (CTRL) and 23 (IUGR) miRNAs, were differentially expressed between males and females (p<0.05) suggesting sexual dimorphism, which can be at least partially explained by differential expression of upstream transcription factors (e.g. HNF4a, and NF?B p50). Lipidomics analysis of fetal cardiac tissue exhibited a net increase in diacylglycerol and plasmalogens and a decrease in triglycerides and phosphatidylcholines. In summary, IUGR resulting from decreased maternal nutrition is associated with sex-dependent dysregulations in cardiac structure, miRNA expression, and lipid metabolism. If these changes persist postnatally, they may program offspring for higher later life cardiac risk.

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