RNA-seq of mice islets from wt and miR-29a/b-1 pancreatic beta cell specific overexpression transgenic mice
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA637392 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR11928411_1.fastq.gz | Fastqsanger.gz | |||
| SRR11928411_2.fastq.gz | Fastqsanger.gz | |||
| SRR11928412_1.fastq.gz | Fastqsanger.gz | |||
| SRR11928412_2.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 7 |
Similar Datasets
Project description:We investigated the mechanism associated with miR-29 effects by comparing gene expression of whole primary islets isolated from miR-29a/b-1 pancreatic beta cell specific overexpression transgenic mice (βTG mice) and their control littermates by RNA sequencing. Ten-week-old mice were chosen to avoid secondarily affected genes. We identified 346 genes that showed significant differences (p-value < 0.05 and >2-fold change) between the two groups. We then used gene ontology (GO) algorithms to perform functional annotations of these differential genes. The top enriched pathways were linked primarily to inflammatory response, secretory vesicle, and ion channel activity. Islets from the βTG mice showed an enhanced inflammatory response based on an assessment of both the upregulated and the downregulated genes , which suggested a likely positive regulation of phagocytosis (Ahsg), regulation of blood vessel diameter (P2rx1/Kng1/Nos2), and monocyte chemotaxis (Cxcl10/Cxcl17).
2020-06-05 | GSE151844 | GEO
Project description:miR-29a/b1 was reported to be involved in the regulation of reproductive function in female mice, but the underlying molecular mechanisms were not clear. In this study, female mice lacking miR-29a/b1 showed a delay in vaginal opening, irregular estrus cycles, ovulation disorder and infertility. However, the development of egg was normal in mutant mice and the ovulation disorder could be rescued by the superovulation treatment. The plasma level of luteinizing hormone (LH) was significantly lower in the mutant mice. Using iTRAQ coupled with LC-MS/MS, we found that the deficiency of miR-29a/b1 in mice resulted in an abnormal expression of a number of proteins involved in vesicular transport and secretion in the pituitary gland. The miR-29a/b1 targeting gene Dnmt3a and Hdac4 were up-regulated in the pituitary of miR-29a/b1 knockout mice suggesting that these two epigenetic writers may be the upstream causes for these phenotype changes due to miR-29a/b1 deficiency. These findings demonstrated that miR-29a/b1 is indispensable for the function of the reproductive axis through regulating LH secretion in the pituitary gland.
2021-09-09 | PXD017106 | Pride
Project description:The aim of this study was to determine the effect of transgenic Aire expression on the transcriptional profile of a tissue that normally does not express Aire: pancreatic islets. The transcriptional profile of transgenic RIP-Aire27 islets was compared to non-transgenic littermate islets as well as to archival NOD thymic medullary epithelial cells (MEC) data. All data were from non-obese diabetic (NOD) mice Keywords: RIP-Aire transgenic vs non-transgenic comparison
2008-08-20 | GSE12073 | GEO
Project description:To confirm the mechanism of miR-29a in liver fibrosis healing, we have employed whole genome microarray expression profiling as a discovery platform to identify genes. CCl4 and TAA liver fibrosis model mouse were used for this experiment. After five weeks liver fibrosis induction period, mouse have been observed for one week (1w) or two weeks (2w) and negative control nucleotide (N.C) or miR-29a were injected every 3 days on this period. We used CCl4 1w N.C (n = 1), 1w miR-29a (n = 1), 2w N.C (n = 1), 2w miR-29a (n = 1), and also used TAA model mouse (total n = 8) liver samples for microarray analysis. We can get only one gene (PDGF-c) as a target of miR-29a which relate to liver fibrosis and down-regulated more than 1.5 times in common miR-29a injected group than N.C group.
2015-03-31 | GSE67423 | GEO
Project description:To confirm the mechanism of miR-29a in liver fibrosis healing, we have employed whole genome microarray expression profiling as a discovery platform to identify genes. CCl4 and TAA liver fibrosis model mouse were used for this experiment. After five weeks liver fibrosis induction period, mouse have been observed for one week (1w) or two weeks (2w) and negative control nucleotide (N.C) or miR-29a were injected every 3 days on this period. We used CCl4 1w N.C (n = 1), 1w miR-29a (n = 1), 2w N.C (n = 1), 2w miR-29a (n = 1), and also used TAA model mouse (total n = 8) liver samples for microarray analysis. We can get only one gene (PDGF-c) as a target of miR-29a which relate to liver fibrosis and down-regulated more than 1.5 times in common miR-29a injected group than N.C group. CCl4 and TAA liver fibrosis model mouse were used for this experiment. After five weeks liver fibrosis induction period, mouse have been obserbed for one week (1w) or two weeks (2w) and negative control nucleotide (N.C) or miR-29a were injected every 3 days on this period. We used CCl4 1w N.C (n = 1), 1w miR-29a (n = 1), 2w N.C (n = 1), 2w miR-29a (n = 1), and also used TAA model mouse (total n = 8) liver samples for microarray analysis.
2015-03-31 | E-GEOD-67423 | biostudies-arrayexpress
Project description:The aim of this study was to determine the effect of transgenic Aire expression on the transcriptional profile of a tissue that normally does not express Aire: pancreatic islets. The transcriptional profile of transgenic RIP-Aire27 islets was compared to non-transgenic littermate islets as well as to archival NOD thymic medullary epithelial cells (MEC) data. All data were from non-obese diabetic (NOD) mice Experiment Overall Design: 3-wk-old individual male RIP-Aire27 or non-transgenic littermates islets were isolated by gradient purification followed by hanpicking under a microscope for subsequent RNA purification, labeling and hybridization to Affymetrix arrays.
2008-10-25 | E-GEOD-12073 | biostudies-arrayexpress
Project description:RNA-seq of primary islets in WT and Brsk2 transgenic mice
| PRJNA637638 | ENA
Project description:To elucidate the role of pericytic cytokines in islet inflammation, we interfered with the expression of MyD88, a key modulator of the IL1R1/TLR pathway, in pericytes using transgenic mice (Nkx3.2-Cre;MyD88 flox/flox) . To determine the impact on islet immune cells, we isolated CD45+ cells from the islets of both non-transgenic and Myd88-deficient mice via MACS, pooling samples from 4-5 littermate male mice. Additionally, unsorted islet cells from the same pool were included to meet the cell number requirements for sample preparation using X10 genomics.
2023-12-31 | E-MTAB-13640 | biostudies-arrayexpress
Project description:Age-related hearing loss (ARHL) is the most common sensory degenerative disease and can significantly impact the quality of life in elderly people. A previous study using GeneChip miRNA microarray assays showed that the expression of miR-29a changes with age, however, its role in hearing loss is still unclear. In this study, we characterized the cochlear phenotype of miR-29a knockout (miR-29a-/-) mice and found that miR-29a-deficient mice had a rapid progressive elevation of the hearing threshold from 2 to 5 months of age compared with littermate controls as measured by the auditory brainstem response. Stereocilia degeneration, hair cell loss and abnormal stria vascularis were observed in miR-29a-/- mice at 4 months of age. Transcriptome sequencing results showed elevated extracellular matrix (ECM) gene expression in miR-29a-/- mice. Both GO annotation and KEGG pathway enrichment analysis revealed that the key differences were closely related to ECM. Further examination with a transmission electron microscope showed thickening of the basilar membrane in the cochlea of miR-29a-/- mice. Five Col4a genes (Col4a1-a5) and two laminin genes (Lamb2 and Lamc1) were validated as miR-29a direct targets by dual luciferase assays and miR-29a inhibition assays with a miR-29a inhibitor. Consistent with the target gene validation results, the expression of these genes was significantly increased in the cochlea of miR-29a-/- mice, as shown by RT-PCR and Western blot. These findings suggest that miR-29a plays an important role in maintaining cochlear structure and function by regulating the expression of collagen and laminin and that the disturbance of its expression could be a cause of progressive hearing loss.
2023-04-11 | GSE228284 | GEO
Project description:Changes in mRNA transcripts in retina of miR-29a knockout mice
| PRJNA773562 | ENA