Gallus gallus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA116243 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:MicroRNA (miRNA) is a family of small regulatory RNA that post-transcriptionally regulates many biological functions including growth and development. Chicken miR-143 and miR-10a are expressed in both the embryonic and post-hatch chick in a spatio-temporal manner. In order to study the functions of these miRNAs, loss of function and microarray approaches were employed. Spleen cells were isolated from embryonic day 18 chickens and immediately transfected with either a synthetic miR-143 inhibitor or a synthetic miR-10a inhibitor or a negative control oligo-nucleotide (Dharmacon). Cultures were maintained for 48 hrs and microarray analysis was performed using the Arizona Gallus gallus 20.7K long oligoarray (GPL6049). Differentially expressed genes were identified for each miRNA by comparing the miRNA knock-down group to the negative control group. The differentially expressed genes were functionally categorized using the DAVID Functional Annotation Tool (http://david.abcc.ncifcrf.gov/). The 3’-UTR of the up-regulated genes (de-repressed after the miRNAs knock-down) were scanned for potential miR-143 or miR-10a binding sites using the miRanda algorithm version 3.1 (http://www.microrna.org/microrna). In addition, the Chicken (Gallus gallus) Unigene database (NCBI) was also used to predict potential targets of these miRNAs. A set of predicted targets for both miRNAs was selected and validated by dual luciferase reporter gene assay. Overall, many of the identified targets for miR-143 are associated with cell proliferation, tumerigenesis and apoptosis. Many of potential targets for miR-10a are associated with immune response.
2010-01-01 | GSE16653 | GEO
Project description:MicroRNA (miRNA) is a family of small regulatory RNA that post-transcriptionally regulates many biological functions including growth and development. Chicken miR-143 and miR-10a are expressed in both the embryonic and post-hatch chick in a spatio-temporal manner. In order to study the functions of these miRNAs, loss of function and microarray approaches were employed. Spleen cells were isolated from embryonic day 18 chickens and immediately transfected with either a synthetic miR-143 inhibitor or a synthetic miR-10a inhibitor or a negative control oligo-nucleotide (Dharmacon). Cultures were maintained for 48 hrs and microarray analysis was performed using the Arizona Gallus gallus 20.7K long oligoarray (GPL6049). Differentially expressed genes were identified for each miRNA by comparing the miRNA knock-down group to the negative control group. The differentially expressed genes were functionally categorized using the DAVID Functional Annotation Tool (http://david.abcc.ncifcrf.gov/). The 3â-UTR of the up-regulated genes (de-repressed after the miRNAs knock-down) were scanned for potential miR-143 or miR-10a binding sites using the miRanda algorithm version 3.1 (http://www.microrna.org/microrna). In addition, the Chicken (Gallus gallus) Unigene database (NCBI) was also used to predict potential targets of these miRNAs. A set of predicted targets for both miRNAs was selected and validated by dual luciferase reporter gene assay. Overall, many of the identified targets for miR-143 are associated with cell proliferation, tumerigenesis and apoptosis. Many of potential targets for miR-10a are associated with immune response. A reference designed microarray was performed in which samples (Cy3) were co-hybridized with the reference RNA pool (Cy5) on the array. The microarray data set was processed using within- and across-array loess normalization method in JMP Genomics 3.0, SAS (Cary, NC). Data quality was evaluated using the MA plots process and the correlation and grouped scatter plots procedure (JMP Genomics 3.0). Differentially expressed genes were identified using ANOVA process on JMP Genomics 3.0 with fixed effect of treatments and random effect of arrays.
2010-05-16 | E-GEOD-16653 | biostudies-arrayexpress
Project description:Retinal neovascularization is a severe complication of several neovascular retinal diseases, including proliferative diabetic retinopathy, central retinal vein occlusion and retinopathy of prematurity. MicroRNAs (miRNAs) are master regulators of gene expression that play an important role in retinal neovascularization. Here, we investigate the retinal miRNA expression profile in a rat model of oxygen-induced retinopathy (OIR) using miRNA-Seq. We show that miR-143-3p, miR-126-3p, and miR-150-5p are significantly downregulated in the retina of OIR rats, and intravitreal injection of synthetic mimics of these miRNAs significantly ameliorate retinal neovascularization in this animal model. Of these identified miRNAs, miR-143 which is highly expressed in the neural retina and retinal vasculature is here identified for the first time to be associated with retinal neovascularization. With a focus on miR-143 expression in primary human retinal endothelial cells, we explore its involved pathways through a multi-omics analysis. In miR-143 treated cells, the functional evaluation showed a decrease in cell migration and delayed endothelial vessel-like tube remodelling. Consequently, the multi-omics analysis suggests that miR-143 negatively impacts endothelial cell activity through regulating cell-matrix adhesion and mediating HIF signalling pathway. Furthermore, using cytoHubba, a topological analysis method to assess the essentiality of genes, we predict 20 top hub genes regulated by miR-143 that may be involved in mediating endothelial cell function. Using CIBERSORTx, a bulk gene expression deconvolution algorithm, we analyze a public RNA-Seq dataset (GSE102485) and demonstrate that the retinal neovascular membranes in patients with proliferative diabetic retinopathy (PDR) principally consist of endothelial cells. We then identify 2 hub genes, THBS1 and SERPINE1, direct targets of miR-143, which on further analysis demonstrate an expression level significantly altered in the PDR patients compared to controls. These findings suggest that miR-143 appears to be essential for limiting endothelial cell-matrix adhesion, thus suppressing retinal neovascularization. The present study might have important implications for the exploration of potential therapeutic targets for the treatment of neovascular ocular diseases.
2026-06-29 | PXD029706 | Pride
Project description:It seems established that genetic and epigenetic determinants drive the multifactorial pathogenic processes in vulvar lichen sclerosus (VLS). Aberrant expression of microRNAs (miRNAs) has been observed in a few studies suggesting potential involvement. We aimed to assess the expression of miRNAs both in VLS and in healthy keratinocytes and fibroblasts cultured separately. The differential analysis led to the identification of 171 and 111 microRNAs with an expression difference of at least 1.5-fold between VLS and healthy samples, in keratinocytes and fibroblasts, respectively. More than 80% of the 111 microRNAs identified as differentially expressed in fibroblasts were also found to be differentially expressed in keratinocytes. A number of dysregulated miRNAs are involved in inflammation and fibrotic processes, namely miR-10a-5p and 3p, miR-143-3p and 5p, miR-181a-5p and 3p, miR-181b-5p and 3p, miR-21-3p, miR-146b-5p and miR-29c. Our results showed a clear separation of VLS keratinocytes and fibroblasts from healthy cells in terms of miRNA expression. It is noteworthy that the most dysregulated miRNAs are implicated in inflammatory and fibrotic pathways. It is conceivable that miRNA expression is functional in regulating pathogenetic mechanisms of LS.
2023-12-13 | GSE249675 | GEO
Project description:The aim of this study was to detect and functionally investigate miRNAs linked to insulin sensitivity in human subcutaneous white adipose tissue (scWAT). Subjects were selected based on the insulin-stimulated lipogenesis response of subcutaneous adipocytes. Eleven miRNAs displayed differential expression between OIR and OIS states. Overexpression of miR-143-3p and miR-652-3p increased insulin-stimulated lipogenesis in human in vitro-differentiated adipocytes. MicroRNAs-143-3p and -652-3p are linked to scWAT insulin resistance independently of obesity.
2017-05-01 | GSE87379 | GEO
Project description:Breast cancer (BC) is a commonly identified life-threatening type of cancer and a major cause of death among women worldwide. Several microRNAs (miRs), including miR-143-5p, have been reported to be vital for regulating hallmarks of cancer; however, the effect of miR-143-5p on BC requires further exploration. The present study performed bioinformatics analysis on GSE42072 and GSE41922 datasets from the National Center for Biotechnology Information Gene Expression Omnibus (GEO) database to identify miR-143-5p expression patterns. Furthermore, miR-143-5p expression was detected in BC cell lines and tissues via reverse transcription-quantitative PCR. Post-transfection with miR-143-5p mimics, Cell Counting Kit-8, colony formation and Transwell assays were performed to explore the effects of miR-143-5p on BC cell proliferation, colony formation, and migration. The association of miR-143-5p with the hypoxia-inducible factor-1α (HIF-1α)-associated glucose transporter 1 (GLUT1) pathway was explored via western blotting, immunofluorescence and dual-luciferase reporter assay. The present study detected high expression of miR-143-5p in BC tissue of the GSE42072 and serum of the GSE41922 datasets by GEO chip analysis. Additionally, the expression levels of miR-143-5p were decreased in BC tissues compared with those in adjacent healthy tissues, and low miR-143-5p expression was associated with a poorer prognosis and shorter survival time in patients with BC. In vitro, miR-143-5p expression levels were decreased in BC cells, and transfection with miR-143-5p mimics suppressed BC cell proliferation, colony formation, migration. Furthermore, miR-143-5p targeted the HIF-1α-related GLUT1 pathway, and inhibited HIF-1α and GLUT1 expression. Additionally, HIF-1α agonists reversed the miR-143-5p-induced inhibition during tumorigenesis. In conclusion, miR-143-5p exhibited low expression in BC tissues, and suppressed BC cell proliferation, colony formation, migration. Moreover, the antitumor effects of miR-143-5p targeted the HIF-1α-related GLUT1 pathway.
2022-02-26 | E-MTAB-11160 | 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.
2011-04-08 | GSE26460 | GEO
Project description:MicroRNAs (miRNAs) are small RNAs that function as post-transcriptional regulators of gene expression. miRNAs affect a variety of signaling pathways and impaired miRNA regulation may contribute to the development of cancer and other diseases. We show that miRNA miR-10a interacts with the 5' untranslated region of mRNAs encoding ribosomal proteins and enhances their translation. miR-10a alleviates translational repression of the ribosomal protein mRNAs during amino acid starvation and is required for their stress-mediated activation following anisomycin treatment. miR-10a binds immediately downstream of the regulatory 5' TOP motif and the 5´TOP is necessary for miR-10a translational enhancement. The results indicate that miR-10a may positively control global protein synthesis via stimulation of ribosomal protein mRNA translation and that the 5' TOP regulatory complex and miR-10a are functionally interconnected.
2008-11-08 | E-MEXP-1375 | biostudies-arrayexpress
Project description:MicroRNAs (miRNAs) have emerged as important gene regulators and are recognized as key players in tumorigenesis. miR-143 is reported to be down-regulated in several cancers, but knowledge of its targets in colon cancer remains limited. To investigate the role of miR-143 in colon cancer, we have employed a microarray based approach to identify miR-143 targets. Based on seed site enrichment analyses and unbiased word analyses, we found a significant enrichment of miRNA binding sites in the 3’-untranslated regions (UTRs) of transcripts down-regulated upon miRNA overexpression. Here we identify Hexokinase 2 (HK2) as a direct target of miR-143 and show that re-introduction of miR-143 in the colon cancer cell line DLD-1 results in a decreased lactate secretion, indicating that miR-143 down-regulation of HK2 affects glucose metabolism in colon cancer cells.
2012-05-02 | GSE33420 | GEO
Project description:We performed RNA sequencing (RNA-seq) on cervical tissues from 3 patients with SCC (IB stage, HPV16-positive) and 3 normal controls (HPV16-negative). Differential gene expression, functional enrichment, and protein-protein interaction (PPI) network analyses were conducted to screen key microRNAs (miRNAs) and target genes. Expression of miR-143-3p and SLC7A11 in SCC and normal control tissues was determined by quantitative real-time polymerase chain reaction (qRT-PCR), immunohistochemical staining, and Western blotting (WB). Furthermore, the effect of miR-143-3p mimics and inhibitors on cell proliferation and ferroptosis was evaluated via Cell Counting Kit (CCK)-8 and scratch assays, along with WB, while concurrently detecting ferroptosis-related biochemical markers. Finally, the role of miR-143-3p in epithelial-mesenchymal transition (EMT) of cervical cancer cells was evaluated by WB and immunofluorescence.
2026-07-31 | E-MTAB-17403 | biostudies-arrayexpress