Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA308569 | ENA |
REPOSITORIES: ENA
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Project description:MicroRNAs (miRNAs) are small noncoding RNAs that critically regulate gene expression. Their abundance and function have been linked to processes such as senescence and aging. In aged monkey muscle, miR-451a and miR-144-3p were highly upregulated compared to young animals. This led us to hypothesize that the miRNAs 451a/144-3p may be involved in muscle differentiation. We found that these miRNAs are downregulated during the differentiation of C2C12 myoblasts. Overexpression of miR-451a, but not miR-144-3p, robustly impeded the differentiation, suggesting an inhibitory role for miR-451a. We further investigated the potential regulatory targets of miR-451a and identified Sparc mRNA, encoding a secreted protein acidic and rich in cysteine (SPARC), which is involved in wound healing and cellular differentiation. Interestingly, we found that miR-451a suppresses Sparc mRNA translation according to the analysis of polysome profile. Our findings show that miR-451a is downregulated in differentiated myoblasts and decreases C2C12 differentiation at least in part by the suppression of SPARC biosynthesis.
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Project description:We have recently confirmed miR-27a-3p as a crucial regulator of human adipogenesis (Wu H, Pula T, Tews D, Amri E-Z, Debatin K-M, Wabitsch M, Fischer-Posovszky P, Roos J. microRNA-27a-3p but Not -5p Is a Crucial Mediator of Human Adipogenesis. Cells. 2021; 10(11):3205. https://doi.org/10.3390/cells10113205 ). MiR-27a-5p did not impair human adipogenesis. However, since several publications state that miR-27a ist also a crucial regulator of UCP1, we were interested if miR-27a-3p or miR-27a-5p regulatas UCP1 and other thermogenesis related genes. We found a strong regulation of UCP1 with functional relevance for the cellular metabolism by miR-27a-5p.To asesse the mRNA gene expression pattern, mRNA sequencing was performed.
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Project description:The prevalence of coronary artery disease (CAD) is increasing among young adults. To improve CAD diagnosis, microRNAs are being explored as potential minimally invasive biomarkers. The aim of this study was to evaluate circulating microRNA (miRNA) expression profiles and assess their value in predicting the development of early-onset CAD. A total of 108 patients with early- and late-onset CAD and 29 individuals without CAD were included, and their miRNA expression was evaluated. The diagnostic value of differentially expressed miRNAs across the subgroups was tested by logistic regression models and ROC curve analysis. A total of 287 different circulating miRNAs were analysed following sequencing and preprocessing. Seven miRNAs (miR-10b-5p, miR-29c-3p, miR-142-5p, miR-320b, miR-451a, miR-486-3p, and miR-625-3p) were found to be differentially expressed across all the study groups, four of which (miR-142-5p, miR-29c-3p, miR-451a, and miR-486-3p) were significantly downregulated in the late-onset CAD group compared with the control group. ROC analysis demonstrated that the combination of the seven miRNAs had high diagnostic accuracy, with an AUC of 0.9924 for distinguishing late-onset CAD from the other groups, and moderate accuracy, with an AUC of 0.8235 for distinguishing early-onset CAD from the other groups. A combination of seven circulating miRNAs (miR-10b-5p, miR-29c-3p, miR-142-5p, miR-320b, miR-451a, miR-486-3p, and miR-625-3p) is a promising biomarker panel for CAD diagnosis, distinguishing between early-onset and late-onset disease. While the panel demonstrated high accuracy in classifying late-onset CAD, its ability to predict early-onset CAD requires further validation. Larger, independent populations are needed to validate the predictive ability of the panel for early disease detection, confirm these findings, and improve generalizability.
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Project description:We investigated the biomolecular activity of miR-29a-3p/miR-223-3p in human lung adenocarcinoma (LUAD) by performing transcriptome profiling of H2023 (LUAD) cell line upon modulation of miR-29a-3p/miR-223-3p by mimic (QIAGEN) (OE) or antisense microRNA (KD).
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Project description:To analyze the effect of miR-223-3p expression on the mRNA level we employed whole genome microarray expression profiling to identify genes with a potential seed region targeted by miR-223-3p. A549 cells were transfected for 48h with either a mirVana miRNA mimic Control or miR-223-3p.
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Project description:Breast Cancer is the cancer with most incidence and mortality in women. microRNAs are emerging as novel prognosis/diagnostic tools. Our aim was to identify a serum microRNA signature useful to predict cancer development. We focused on studying the expression levels of 30 microRNAs in the serum of 96 breast cancer patients versus 92 control individuals. Bioinformatic studies provide a microRNA signature, designated as a predictor, based upon the expression levels of 5 microRNAs. Then, we tested the predictor in a group of 60 randomly chosen women. Lastly, a proteomic study unveiled the over-expression and down-regulation of proteins differently expressed in the serum of breast cancer patients versus that of control individuals. Twenty-six microRNAs differentiate cancer tissue from healthy tissue and 16 microRNAs differentiate the serum of cancer patients from that of the control group. The tissue expression of miR-99a-5p, mir-497-5p, miR-362, and miR-1274, and the serum levels of miR-141 correlated with patient survival. Moreover, the predictor consisting of mir-125b-5p, miR-29c-3p, mir-16-5p, miR-1260, and miR-451a was able to differentiate breast cancer patients from controls. The predictor was validated in 20 new cases of breast cancer patients and tested in 60 volunteer women, assigning 11 out of 60 women to the cancer group. An association of low levels of mir-16-5p with a high content of CD44 protein in serum was found. Circulating microRNAs in serum can represent biomarkers for cancer prediction. Their clinical relevance and use of the predictor here described might be of potential importance for breast cancer prediction.
2020-09-18 | PXD020795 | Pride
Project description:Non-thermal plasma, a partially ionized gas, holds significant potential for clinical applications, including wound healing support, oral therapies, and anti-tumour treatments. While its applications shown promising outcomes, the underlying molecular mechanisms remain incompletely understood. We thus applied non-thermal plasma to mouse auricular skin and conducted non-coding RNA sequencing, as well as single-cell blood sequencing. In a time-series analysis (5 time points spanning 2 hours), we compared the expression of microRNAs in the plasma-treated left ears to the unexposed right ears of the same mice as well as to the ears of unexposed control mice. Our findings indicate specific effects in the treated ears for a set of five miRNAs: mmu-miR-144-5p, mmu-miR-144-3p, mmu-miR-142a-5p, mmu-miR-223-3p, and mmu-miR-451a. Interestingly, miR-223-3p also exhibited an increase over time in the right non-treated ear of the exposed mice, suggesting systemic effects. Notably, this miRNA, along with mmu-miR-142a-5p and mmu-miR-144-3p, regulates genes and pathways associated with wound healing and tissue regeneration (namely ErbB, FoxO, Hippo, and PI3K-Akt signalling). This co-regulation is particularly remarkable considering the significant seed dissimilarities among the miRNAs. Finally, single blood cell sequencing revealed the downregulation of 12 from 15 target genes in B-cells, Cd4+ and Cd8+ T-cells. Collectively, our data provide evidence for a systemic effect of non-thermal plasma.
2023-07-12 | GSE236788 | GEO
Project description:Non-thermal plasma, a partially ionized gas, holds significant potential for clinical applications, including wound healing support, oral therapies, and anti-tumour treatments. While its applications shown promising outcomes, the underlying molecular mechanisms remain incompletely understood. We thus applied non-thermal plasma to mouse auricular skin and conducted non-coding RNA sequencing, as well as single-cell blood sequencing. In a time-series analysis (5 time points spanning 2 hours), we compared the expression of microRNAs in the plasma-treated left ears to the unexposed right ears of the same mice as well as to the ears of unexposed control mice. Our findings indicate specific effects in the treated ears for a set of five miRNAs: mmu-miR-144-5p, mmu-miR-144-3p, mmu-miR-142a-5p, mmu-miR-223-3p, and mmu-miR-451a. Interestingly, miR-223-3p also exhibited an increase over time in the right non-treated ear of the exposed mice, suggesting systemic effects. Notably, this miRNA, along with mmu-miR-142a-5p and mmu-miR-144-3p, regulates genes and pathways associated with wound healing and tissue regeneration (namely ErbB, FoxO, Hippo, and PI3K-Akt signalling). This co-regulation is particularly remarkable considering the significant seed dissimilarities among the miRNAs. Finally, single blood cell sequencing revealed the downregulation of 12 from 15 target genes in B-cells, Cd4+ and Cd8+ T-cells. Collectively, our data provide evidence for a systemic effect of non-thermal plasma.
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Project description:Exosomal microRNAs are closely related to the progression of renal fibrosis. The circadian rhythm gene BMAL1 is thought to be involved in a variety of diseases. However, how BMAL1 regulates renal fibrosis induced by ischemia-reperfusion injury (IRI) has not been determined. We first examined BMAL1 expression, exosomal expression, the macrophage-to-myofibroblast transition (MMT) ratio, and renal fibrosis levels in mice with renal IRI. The results showed that renal IRI induced a decrease in BMAL1 expression, along with an increase in exosome secretion, MMT formation and renal fibrosis. Next, we overexpressed BMAL1 in mouse kidneys and found that BMAL1 inhibited IRI-induced MMT and fibrosis. We confirmed that exosome-mediated MMT directly aggravated renal fibrosis and that this process was directly regulated by BMAL1 through in vivo and in vitro exosome uptake experiments and Rab27a knockout mouse construction. High-throughput miRNA sequencing of exosomes derived from TCMK-1 cells and ChIP assays were used to confirm that exosomal miR-27a-3p was downregulated after hypoxia-reoxygenation (H/R) treatment and that BMAL1 directly promoted the transcription of miR-27a-3p. We identified TGFBR1 as the target gene of miR-27a-3p by transfecting cells with miR-27a-3p mimics and miR-27a-3p inhibitors and performing dual luciferase assays. Finally, we transfected cells with si-TGFBR1 and identified the TGFBR1/smad3 pathway as a key pathway for regulating MMT and renal fibrosis regulated by tubular epithelium-derived exosomal miR-27a-3p. Our findings indicated that BMAL1 was suppressed in renal IRI, which promoted MMT and renal fibrosis by upregulating the level of miR-27a-3p in tubular epithelial-derived exosomes.
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