Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA251871 | ENA |
REPOSITORIES: ENA
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Project description:mRNA profiling of mouse ureters comparing wild-type ureter vs. ureters from mice having whole body deletion of miR-143 and miR-145 which results in abnormal ureter peristalsis and hydronephrosis We used microarrays to detail the global program of gene expression in wild-type and miR-143/145-deficient ureters which revealed dysregulation of genes linked to smooth muscle morphology and function.
2014-10-08 | GSE58274 | GEO
Project description:mRNA profiling of mouse ureters comparing wild-type ureter vs. ureters from mice having whole body deletion of miR-143 and miR-145 which results in abnormal ureter peristalsis and hydronephrosis We used microarrays to detail the global program of gene expression in wild-type and miR-143/145-deficient ureters which revealed dysregulation of genes linked to smooth muscle morphology and function. Two condition experiment: wild type vs miR-143/145 KO; biological replicates: individual mice - 2 wild type, 2 mutant. One replicate per array.
2014-10-08 | E-GEOD-58274 | biostudies-arrayexpress
Project description:Transcriptional profilings of the mouse heart obtained from control (wild-type) and alpha MHC/mir-143/145 transgenic mouse line 9 and 19.
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Project description:In a series of mouse genetic studies, we concluded that miR-143/145 expression in intestinal subepithelial myofibroblasts (ISEMFs) promotes epithelial regeneration after DSS-mediated injury in the colon. This experiment aims to identify miR-143/145 target genes that are involved in this function. We generated primary ISEMFs from wildtype and miR-143/145 null mouse colons and analyzed their gene expression profile. We further subjected ISEMFs to LPS treatment, in order to measure gene expression changes that are only revealed after inflammatory stress. Three wild-type and three miR-143/145 null ISEMF cell lines were isolated from mouse colons. Cells were treated with or without 1 ug/mL LPS for 24 hours and total RNA was isolated. Gene expression was profiled using Illumina microarrays.
2014-05-22 | E-GEOD-55651 | biostudies-arrayexpress
Project description:The contribution of altered posttranscriptional gene silencing (PTGS) to the development of insulin resistance and type 2 diabetes mellitus so far remains elusive. We have described that expression of microRNAs (miR)-143 and -145 is dysregulated in genetic and dietary mouse models of obesity. Induced transgenic overexpression of miR-143, but not miR-145, causes insulin resistance and impaired insulin-stimulated AKT activation. We used microarrays to analyze the underlying molecular mechanisms of miR-143-mediated development of insulin resistance.
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Project description:Mice heart: wild-type mice vs. alpha MHC/mir-143/145 transgenic mice
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Project description:Hypoxia is used as a model for pulmonary arterial hypertension. MiR-145 is upregulated in pulmonary arterial hypertension in humans and female mice. It has been observed that miR-145 knock out mice have reduced vascular remodelling in response to hypoxia. Therefore, knock down of miR-145 could be used as a therapy for pulmonary arterial hypertension in humans. This microarray has helped us to elucidate some of the pathways in the miR-145 knock out mice that may protect against vascular remodelling. Wild type (WT) mice and homozygous miR-145 -/- female mice (strain C57BL6J/129SVEV) at 8 weeks old were exposed to chronic hypoxia for 2 weeks or maintained in normoxic conditions and pulmonary arteries were dissected at 10 weeks of age. This study contained 4 groups, WT hypoxic, WT normoxic, miR-145 -/-, hypoxic miR-145 -/- normoxic each containing 6 animals. All adjacent comparisons were made to ananlyse the data (a 2 by 2 design).
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Project description:In a series of mouse genetic studies, we concluded that miR-143/145 expression in intestinal subepithelial myofibroblasts (ISEMFs) promotes epithelial regeneration after DSS-mediated injury in the colon. This experiment aims to identify miR-143/145 target genes that are involved in this function. We generated primary ISEMFs from wildtype and miR-143/145 null mouse colons and analyzed their gene expression profile. We further subjected ISEMFs to LPS treatment, in order to measure gene expression changes that are only revealed after inflammatory stress.
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Project description:A growing body of literature has proposed cell-autonomous tumor suppressor functions for the mir-143~145 cluster in a variety of human cancers, including lung adenocarcinoma, and has reported therapeutic benefits of delivering mir-143 and mir- 145 to tumors. In contrast to these studies, we found that depletion or forced expression of mir-143 and mir-145 in an autochthonous mouse model of lung adenocarcinoma did not affect tumor development. Surprisingly, we observed that loss of mir-143~145 from the tumor microenvironment significantly reduced tumor burden, indicating a non-cell- autonomous role for these miRNAs in promoting tumorigenesis. By examining the expression patterns of different cell populations isolated in vivo from tumor-bearing lungs using an integrated computational approach, we identified a role for mir-145 in stimulating the proliferation of endothelial cells by downregulating an inhibitory kinase, Camk1d, which prevents mitotic entry. As a consequence, tumors in mir-143~145- deficient animals exhibited diminished hallmarks of neo-angiogenesis, increased apoptosis and their expansion appeared limited by the tumor’s ability to co-opt the alveolar vasculature. These findings show that expression of the mir-143~145 cluster in the tumor stroma promotes rather than suppresses tumorigenesis and cautions against the use of these miRNAs as agents in cancer therapeutics.
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