Analysis of small RNA from exosomes secreted by macrophages infected with Salmonella
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE268198 | GEO | 2026/05/31
REPOSITORIES: GEO
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Project description:Microscale small RNA high-throughput sequencing was used to study small RNA distribution in early zebrafish PGCs (primordial germ cells). We find that early zebrafish PGCs have large quantities of piRNAs and small quantities of miRNAs. Among the miRNAs detected, miR-430 accounted for the majority which has been proved to play diverse roles in zebrafish development. In addition, miR-92a-3p and miR-26a-5p have high expression and previous studies show that these two miRNAs can influence cell proliferation in cancer cells. More experiments should be performed in the future to explore whether miR-92a-3p and miR-26a-5p can influence the number of zebrafish PGCs.
2020-09-13 | GSE157865 | GEO
Project description:MiRNAs regulate posttranscriptional gene expression and are widely implicated in the pathogenesis of complex diseases. We aim to elucidate miRNA regulation of the atrial mRNA signatures that associate with AF. This may provide novel mechanistical insights and candidate targets for therapies using miRNA mimics or antimiRs.
We present combined miRNAs-mRNAs sequencing in atrial tissues of patient without AF (n=22), with paroxysmal AF (n=22) and with persistent AF (n=20). MiRNA and mRNA signatures followed an ordinal scale from nonAF to paroxysmal to persistent AF patients. The previously reported mRNA sequencing identified 5228 differentially expressed genes involved in epithelial to mesenchymal transition, endothelial cell proliferation and extracellular matrix remodelling involving collagens, glycoproteins and proteoglycans. We discovered 103 differentially expressed miRNAs. Key downregulated miRNAs included miR-135b-5p, miR-138-5p, miR-200a-3p, miR-200b-3p and miR-31-5p and key upregulated miRNAs were miR-144-3p, miR-15b-3p, miR-182-5p miR-18b-5p, miR-4306 and miR-206. The expression levels of differentially expressed miRNAs were negatively correlated with the expression levels of their predicted target mRNAs. The downregulated miRNAs demonstrated a more profound transcriptome effect than the upregulated miRNAs. Upregulated biological processes enriched in miRNAs targets related to epithelial and endothelial cell migration and glycosaminoglycan biosynthesis, in line with the processes discovered by the mRNA sequencing analysis.
Combined analysis of miRNA and mRNA sequencing uncovered miRNAs with a broad transcriptional effect in human AF. Epithelial to mesenchymal transition and endothelial cell proliferation were processes controlled by downregulated miR-135b-5p, miR-138-5p, miR-200a-3p, miR-200b-3p and miR-31-5p, which in turn may contribute to (myo)fibroblast activation and structural remodeling.\
| EGAS00001005296 | EGA
Project description:In order to indetify new target genes of miR-92a-1-5p in chronic myeloid leukemia, K562 cells carrying the BCR::ABL1 fusion gene were transiently transfected with miR-92a mimic or scramble and treated with imatinib. RNA was sequenced to identify genes expressed under imatinib treatment and downregulated after miR-92a-1-5p overexpression.
2024-10-11 | GSE278906 | GEO
Project description:The intracellular persistence of Staphylococcus aureus represents a major therapeutic challenge, as it facilitates immune evasion and limits the efficacy of antibiotics with poor intracellular activity. Host-directed therapies based on microRNAs (miRNAs) offer a promising alternative to overcome these limitations. We performed a high-throughput screen of 2,469 human miRNA mimics in S. aureus USA300–infected A549 epithelial cells, followed by network centrality–based prioritization and validation across multiple S. aureus strains and epithelial cell lines. This approach identified ten candidate miRNAs, among which miR-4430, miR-1249-5p, and miR-147a consistently reduced intracellular bacterial burden and improved host cell viability. Host transcriptomic profiling revealed distinct yet complementary mechanisms of action: miR-4430 enhanced innate immune responses, including STAT1- and PTAFR-associated signaling, whereas miR-1249-5p and miR-147a modulated extracellular matrix organization and integrin-mediated adhesion, thereby impairing bacterial entry. Collectively, these miRNAs impose convergent host-driven pressures that restrict intracellular S. aureus proliferation. Our findings highlight the therapeutic potential of miRNA-based host-directed interventions, which could be combined with conventional antibiotics to improve infection control and reduce the emergence of resistance.
2026-02-23 | GSE318734 | GEO
Project description:Post-transcriptional regulation of gene expression by miRNAs likely makes significant contributions to mRNA abundance at the embryo-maternal interface. In this study, we investigated how miR-26a-5p and miR-125b-5p contribute to molecular changes occurring in the uterine luminal epithelium, which serves as the first site of signal exchange between the mother and developing embryo. To measure de novo protein synthesis after miRNA delivery to primary uterine luminal epithelial cells, we employed pulsed stable isotope labeling by amino acids (pSILAC). We found that both miRNAs alter the proteome of luminal epithelial cells, impacting numerous cellular functions, immune responses, as well as intracellular and second messenger signaling pathways. Additionally, we identified several features of miRNA-mRNA interactions that may influence the targeting efficiency of miR-26a-5p and miR-125b-5p. Overall, our study suggests a complex interaction of miR-26a-5p and miR-125b-5p with their respective targets. However, both appear to cooperatively function in modulating the cellular environment of the luminal epithelium, facilitating the morphological and molecular changes that occur during the intensive communication between the embryo and uterus at pregnancy.
2025-05-07 | PXD056243 | Pride
Project description:We tested the hypothesis that a panel of placental mammal-specific miRNAs and their targets play important to establish receptivity to implantation and their dysregulated expression may be a feature in women with early pregnancy loss. Relative expression levels of miR-340-5p, −542-3p, and −671-5p all increased following treatment of Ishikawa cells with progesterone (10 μg/ml) for 24 hrs (p < 0.05). RNA sequencing of these P4-treated cells identified co-ordinate changes to 6,367 transcripts of which 1713 were predicted targets of miR-340-5p, 670 of miR-542-3p, and 618 of miR-671-5p. Quantitative proteomic analysis of Ishikawa cells transfected with mimic or inhibitor (48 hrs: n=3 biological replicates) for each of the P4-regulated miRNAs was carried out to identify targets of these miRNAs. Excluding off target effects, mir-340-5p mimic altered 1,369 proteins while inhibition changed expression of 376 proteins (p < 0.05) of which, 72 were common to both treatments. A total of 280 proteins were identified between predicted (mirDB) and confirmed (in vitro) targets. In total, 171 proteins predicted to be targets by mirDB were altered in vitro by treatment with miR-340-5p mimic or inhibitor and were also altered by treatment of endometrial epithelial cells with P4. In vitro targets of miR-542-3p identified 1,378 proteins altered by mimic while inhibition altered 975 a core of 200 proteins were changed by both. 100 protein targets were predicted and only 46 proteins were P4 regulated. miR-671-mimic altered 1,252 proteins with inhibition changing 492 proteins of which 97 were common to both, 95 were miDB predicted targets and 46 were also P4-regulated. All miRNAs were detected in endometrial biopsies taken from patients during the luteal phase of their cycle, irrespective of prior or future pregnancy outcomes Expression of mir-340-5p showed an overall increase in patients who had previously suffered a miscarriage and had a subsequent miscarriage, as compared to those who had infertility or previous miscarriage and subsequently went on to have a life birth outcome. The regulation of these miRNAs and their protein targets regulate the function of transport and secretion, and adhesion of the endometrial epithelia required for successful implantation in humans. Dysfunction of these miRNAs (and therefore the targets they regulate) may contribute to endometrial-derived recurrent pregnancy loss in women.
2023-05-10 | PXD036109 | Pride
Project description:MiRNAs have been shown to alter both protein expression and secretion in different cellular contexts. By combining in vitro, in vivo and in silico techniques, we demonstrated that overexpression of pre-miR-1307 reduced the ability of breast cancer cells to induce endothelial cell sprouting and angiogenesis. However, the molecular mechanism behind this and the effect of the individual mature miRNAs derived from pre-miR-1307 on protein secretion and is largely unknown. Here, we overexpressed miR-1307-3p|0, -3p|1 and 5p|0 in MDA-MB-231 breast cancer cells and assessed the impact of miRNA overexpression on protein secretion by Mass Spectrometry. Unsupervised hierarchical clustering revealed a distinct phenotype induced by overexpression of miR-1307-5p|0 compared to the controls and to the 5’isomiRs derived from the 3p-arm. Together, our results suggest different impacts of miR-1307-3p and miR-1307-5p on protein secretion which is in line with our in vitro observation that miR-1307-5p, but not the isomiRs derived from the 3p-arm reduce endothelial cell sprouting in vitro. Hence these data support the hypothesis that miR-1307-5p is at least partly responsible for impaired vasculature in tumors overexpressing pre-miR-1307.
2024-12-11 | PXD041087 | Pride
Project description:Patients with advanced colorectal cancer (CRC) are commonly treated with systemic combination therapy but suffer eventually from drug resistance. MicroRNAs (miRNAs) are suggested to play a role in treatment resistance of CRC. We studied whether restoring downregulated miR-195-5p and 497-5p sensitize CRC cells to currently used chemotherapeutics 5-fluorouracil, oxaliplatin and irinotecan. Sensitivity to 5-FU, oxaliplatin and irinotecan before and after transfection with miR-195-5p and miR-497-5p mimics was analyzed in CRC cell lines HCT116, RKO, DLD-1 and SW480. Mass spectrometry based proteomic analysis of transfected and wild-type cells was used to identify targets involved in sensitivity to chemotherapy. Proteomic analysis revealed 181 proteins with significantly altered expression after transfection with miR-195-5p mimic in HCT116 and RKO, including 118 downregulated and 63 upregulated proteins. After transfection with miR-497-5p mimic, 130 proteins were significantly downregulated and 102 were upregulated in HCT116 and RKO (P<0.05 and FC<-3 or FC>3). CHUK and LUZP1 were coinciding downregulated proteins in sensitized CRC cells after transfection with either mimic. Resistance mechanisms of these two proteins may be related to nuclear factor kappa-B signaling and G1 cell cycle arrest, respectively. Restoring miR-195-5p and miR-497-5p expression enhanced sensitivity to chemotherapy, mainly oxaliplatin, in CRC cells and could be a promising treatment strategy for patients with mCRC. Proteomics revealed potential targets of these miRNAs involved in sensitivity to chemotherapy.
2019-09-27 | PXD015369 | Pride
Project description:Abstract Objectives: Abdominal aortic aneurysm (AAA) is a fatal cardiovascular disease with no effective drug treatment currently available. The aberrant expressions of microRNAs (miRNAs) contribute to AAA pathogenesis. In this study, we aimed to perform miRNA microarray analysis to screen for differentially expressed miRNAs in the aortas of AAA mice compared to those in control mice, and to clarify the role and mechanism of miRNA-378a-5p (miR-378a-5p) in the AAA development. Methods: We performed a comprehensive miRNA microarray analysis to screen for differentially expressed miRNAs in the aortas of AAA mice and control mice. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expressions of miR-378a-5p in the serum and aortas of AAA patients and mice. To clarify the role of miR-378a-5p in the AAA development in vivo, miR-378a-5p antagomir and angomir were administered to ApoE-/- mice using tail venous injection, followed by Angiotensin II (Ang II) infusion. Next, the role of miR-378a-5p in the phenotypic switching and migration of vascular smooth muscle cells (VSMCs) was examined in vivo and in vitro. Mechanistically, the targets of miR-378a-5p were identified by bioinformatics analysis, luciferase assay, qRT-PCR and western blot. Co-immunoprecipitation (Co-IP) assay combined with mass spectrometry were carried out for excavating potential downstream effectors. Results: The expression of miR-378a-5p was decreased in the serum and aortas of AAA patients and mice, and tumor necrosis factor-α (TNFα)-treated VSMCs. In vivo, the antagomir-378a-5p aggravated AAA formation, as evidenced by a larger maximal aortic diameter and greater medial elastin degradation than in control mice. MiR-378a-5p angomir had the opposite effect. In vitro, miR-378a-5p overexpression significantly promoted the contraction ability and suppressed the migration of VSMCs, whereas miR-378a-5p knockdown inhibited the contraction ability and increased the migration of VSMCs. Mechanistically, we discovered that miR-378a-5p played a protective role in AAA development by regulating actin-binding LIM protein 1 (ABLIM1)-megakaryoblastic leukemia 1 (MKL1) pathway. Conclusion: MiR-378a-5p exerts protective effects against AAA by maintaining VSMCs homeostasis via the ABLIM1-MKL1 pathway. Therefore, targeting miR-378a-5p may be an attractive therapeutic strategy for AAA treatment.
2026-01-13 | PXD073033 |
Project description:miR-493-5p, miR-3662, and miR-589-3p were estimated as working microRNAs in bleomycin- and methotrexate-induced phenotypic changes in A549 cells via microRNAs-Proteins Analysis of Integrative Relationship (miR-PAIR). To verify the effect of these miRNAs on the their target protein expression levels, comprehensive expression of proteins in A549 cells treated with miR-493-59, miR-3662, and miR-589-3p mimic was examined by SWATH-MS method. As expected by a miR-PAIR mehtod, almost target proteins were succesfully regulated by miR-493-5p and miR-589-3p mimics.
2025-07-25 | PXD053397 | Pride