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Expression of miR-381-3p is elevated in the retina of OIR mice, but the role in the retinal neovascularization is elusive，and its mechanism of action was investigated by vitreous injection of miR-381-3p antagomir

ABSTRACT: To investigate the mechanism of miR-381-3p in the OIR mice retinal tissues OIR mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE231376 | GEO | 2023/05/05

REPOSITORIES: GEO

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ADAR1 controls the miR-381-3p-mediated expression of MRP4 by regulating the production of circHIPK3 in human renal cell

Project description:Multidrug resistance-associated protein 4 (MRP4), a member of the C subfamily of ATP-binding cassette transporters, is highly expressed in the kidney of mammals and responsible for renal elimination of various drugs. Adenosine deaminase acting on RNA 1 (ADAR1) has been reported to regulate gene expression through catalyzing adenosine-to-inosine (A-to-I) RNA editing. In this study, we found that the down-regulation of ADAR1 increased the expression of MRP4 in human renal cells at post-transcriptional level. The results of luciferase reporter assays and microarray analysis revealed that down-regulation of ADAR1 decreased the levels of miR-381-3p, which led to the up-regulation of MPR4 expression. Circular RNAs (circRNAs) are a kind of closed loop endogenous non-coding RNAs that play a critical role of gene expression by acting as miRNA sponges. ADAR1 repressed the biogenesis of circular RNA circHIPK3 by catalyzing A-to-I RNA editing, which changed the secondary structure of precursor of circHIPK3. In silico analysis suggested that circHIPK3 acted as a sponge of miR-381-3p. Indeed, overexpression of circHIPK3 up-regulated the expression of MRP4 through interfering with miR-381-3p. Our results provide the novel point of view for regulating mechanism of the expression of xenobiotic transporters through mediating the control of circRNA expression by RNA editing enzyme ADAR1.

2022-07-27 | GSE192692 | GEO

Impact of miR-132 and miR-381 on endogenous forskolin responsive CREB targets in HEK293T cells

Project description:Expression profiling of HEK293T cells transfected with miR-neg (negative control), miR-132 or miR-381 mimics and treated with forskolin for 0, 1 or 4hrs.

2011-07-01 | GSE24812 | GEO

Gene expression microarray analysis of early oxygen-induced retinopathy (OIR)

Project description:Different inbred strains of rats differ in their susceptibility to OIR, an animal model of human retinopathy of prematurity. We examined gene expression profiles in Fischer 344 (F344, resistant to OIR) and Sprague Dawley (SD, susceptible to OIR) rats at the early time point of day 3 to identifying gene pathways related to the underlying genetic cause of phenotypic differences between strains. To examine gene expression changes in rats strains which are resistant and susceptible to OIR, four different experimental conditions were analysed: F344 cyclic hyperoxia (O2) exposed, F344 room air (RA) exposed, SD O2 exposed and SD RA exposed. A minimum of two samples of pooled RNA, comprising of 3 individual rats from 2 separate litters, was used for each experimental condition. Pooled RNA from different rats were used as biological replicates. An additional sample for F344 O2 and SD RA rats was included on the basis of the principal components analysis from the initial 8 samples. Pooled RNA from age-matched room air-exposed rats were used as controls.

2009-11-12 | E-GEOD-18998 | biostudies-arrayexpress

Expression profiles of mRNAs in the retinas of OIR wildtype, OIR IL-19 knockout and room air control mice.

Project description:Seven-day-old C57BL/6 mice and IL-19 knockout (KO) mice were subjected to 75% oxygen for 5 days to induce OIR. To explore the mechanism that caused by IL-19 on retinal neovascularization, Gene expressions among retinas of room air control mice, OIR wildtype mice, and OIR IL-19 knockout mice were measured by RNA-sequencing (RNA-seq).

2022-01-24 | GSE194176 | GEO

Gene expression microarray analysis of early oxygen-induced retinopathy (OIR)

2009-11-13 | GSE18998 | GEO

Impact of miR-132 and miR-381 on endogenous forskolin responsive CREB targets in HEK293T cells

Project description:Expression profiling of HEK293T cells transfected with miR-neg (negative control), miR-132 or miR-381 mimics and treated with forskolin for 0, 1 or 4hrs. HEK293T cells were reverse transfected with the respective miRNA mimics. 72hrs post-transfection, cells were treated with forskolin for 0, 1 or 4hrs. Total RNA was then extracted. Expression profiling was carried out with Affymetrix arrays. Experiment was performed in duplicate. Total of 18 samples.

2011-07-01 | E-GEOD-24812 | biostudies-arrayexpress

Porphyromonas gingivalis 381

Project description:Porphyromonas gingivalis 381 Genome sequencing

| PRJNA220980 | ENA

Knockdown of SETDB1 inhibits breast cancer progression by miR-381-3p-related regulation.

Project description:BACKGROUND:SET domain bifurcated 1 (SETDB1) has been widely considered as an oncogene playing a critical role in many human cancers, including breast cancer. Nevertheless, the molecular mechanism by which SETDB1 regulates breast cancer tumorigenesis is still unknown. METHODS:qRT-PCR assay or western blot analysis was performed to assess the expression level of SETDB1 mRNA or protein, respectively. siSETDB1, pCMV6-XL5-SETDB1, miR-381-3p mimic, or miR-381-3p inhibitor was transfected into cells to regulate the expression of SETDB1 or miR-381-3p. MiRNA directly interacted with SETDB1 was verified by luciferase reporter assay and RNA immunoprecipitation. CCK-8 assay, colony formation assay, flow cytometric analysis, and transwell assay were used to detect the abilities of cell proliferation, cell cycle progression and migration, respectively. Animal model of xenograft tumor was used to observe the regulatory effect of SETDB1 on tumor growth in vivo. RESULTS:We verified that SETDB1 mRNA level was upregulated in breast cancer tissues and cell lines, and SETDB1 depletion led to a suppression of cell proliferation, cell cycle progression and migration in vitro, as well as tumor growth in vivo. SETDB1 was verified to be a target of miR-381-3p. Moreover, miR-381-3p overexpression suppressed cell proliferation, cell cycle progression and migration, whereas SETDB1 abated miR-381-3p-mediated regulatory function on breast cancer cells. CONCLUSIONS:This study revealed that SETDB1 knockdown might suppress breast cancer progression at least partly by miR-381-3p-related regulation, providing a novel prospect in breast cancer therapy.

| S-EPMC6180515 | biostudies-other

Use of microarray analyses to determine the effect of hyperoxia and hypoxia on gene expression in early oxygen-induced retinopathy (OIR).

Project description:Different inbred strains of rats differ in their susceptibility to OIR, an animal model of human retinopathy of prematurity. We examined gene expression profiles in Fischer 344 (F344, resistant to OIR) and Sprague Dawley (SD, susceptible to OIR) rats at the early time points of day 5 (in response to hyperoxia) and day 6 (in response to relative hypoxia) to identify gene pathways related to the underlying genetic cause of the phenotypic differences observed between strains. To examine gene expression changes in rat strains which are resistant and susceptible to OIR, four different experimental conditions were analysed: F344 cyclic hyperoxia (O2) exposed, F344 room air (RA) exposed, SD O2 exposed and SD RA exposed. Two samples of pooled RNA, comprising of 3 individual rats from 2 separate litters, was used for each experimental condition, for each time point of interest. Pooled RNA from age-matched room air-exposed rats were used as controls.

2012-02-24 | E-GEOD-36037 | biostudies-arrayexpress

miR-381-3p Involves in Glioma Progression by Suppressing Tumor-Promoter Factor ANTXR1.

Project description:Accumulating studies revealed association between development of glioma and miRNA dysregulation. A case in point is miR-381-3p, but its mechanism in glioma is unclear yet. In this work, we confirmed that overexpressed miR-381-3p repressed biological functions of glioma cells. Additionally, we also discovered that upregulated anthrax toxin receptor 1 (ANTXR1) was negatively mediated by miR-381-3p. We further proved that miR-381-3p-targeted ANTXR1 was able to counteract the suppression of miR-381-3p on biological functions of glioma. We concluded that miR-381-3p and ANTXR1 were both important factors in modulating glioma progression. miR-381-3p/ANTXR1 axis is expected to be a molecular target for glioma.

| S-EPMC8702332 | biostudies-literature

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