Similar Datasets
Project description:Mitochondria were isolated from skeletal muscle and the remaining tissue fraction was collected to identify RNA enriched in mitochondria.
2024-03-15 | GSE235762 | GEO
Project description:Mitochondria were isolated from brown adipose tissue and the remaining tissue fraction was collected to identify RNA enriched in mitochondria.
2024-03-15 | GSE235759 | GEO
Project description:Small noncoding RNAs (ncRNAs), particularly miRNAs, play key roles in a plethora of biological processes both in health and disease. Although largely operative in the cytoplasm, emerging data indicate their shuttling in different subcellular compartments. Given the central role of mitochondria in cellular homeostasis, here we systematically profiled their small ncRNAs content across mouse tissues that largely rely on mitochondria functioning. The ubiquitous presence of piRNAs in mitochondria (mitopiRNA) of somatic tissues is reported for the first time, supporting the idea of a strong and general connection between mitochondria biology and piRNA pathways. Then, we found groups of tissue-shared and tissue-specific mitochondrial miRNAs (mitomiRs), potentially related to the “basic” or “cell context dependent” biology of mitochondria. Overall, this large data platform will be useful to deepen the knowledge about small ncRNAs processing and their governed regulatory networks contributing to mitochondria functions.
2023-09-01 | E-MTAB-12911 | biostudies-arrayexpress
Project description:MicroRNAs (miRNAs) are small non-coding RNAs that associate with Argonaute 2 protein to regulate gene expression at the post-transcriptional level in the cytoplasm. However, recent studies have reported that some miRNAs localize to and function in other cellular compartments. Mitochondria harbour their own genetic system that may be a potential site for miRNA-mediated post-transcriptional regulation. We aimed at investigating whether nuclear-encoded miRNAs can localize to and function in human mitochondria. To enable identification of mitochondrial-enriched miRNAs, we profiled the mitochondrial and cytosolic RNA fractions from the same HeLa cells by miRNA microarray analysis. Mitochondria were purified using a combination of cell fractionation and immunoisolation, and assessed for the lack of protein and RNA contaminants. We found 57 miRNAs differentially expressed in HeLa mitochondria and cytosol. Of these 57, a signature of 13 nuclear-encoded miRNAs was reproducibly enriched in mitochondrial RNA and validated by RT-PCR for hsa-miR-494, hsa-miR-1275 and hsa-miR-1974. This study provides the first comprehensive view of the localization of RNA interference components to the mitochondria. Our data outline the molecular bases for a novel layer of crosstalk between nucleus and mitochondria through a specific subset of human miRNAs that we termed ‘mitomiRs’. To assess whether nuclear-encoded miRNA are detectable in human mitochondria, we performed the following four steps approach. First, cultured HeLa cells were allowed to reach 80-100% confluence and subjected to fractionation in order to isolate the cytosolic fraction. From the same HeLa cells, mitochondria were isolated by immunomagnetic Anti-TOM22 MicroBeads from the Mitochondria Isolation Kit (Miltenyi Biotec). In total, six mitochondria preparations were perfromed, three of these were additionally treated with RNase A. Second, total RNA was extracted from the mitochondrial and cytosolic fractions. Third, mitochondrial and cytosolic RNA were respectively profiled by microRNA microarray analysis. Last, data were analyzed and normalized.Three independent assays were performed.
2011-10-05 | E-GEOD-24761 | biostudies-arrayexpress
Project description:Heart failure (HF) with preserved ejection fraction (HFpEF) is rising, whose morbidity, mortality and healthcare costs are similar to HF with reduced ejection fraction (HFrEF). Although substantial molecular pathways lead to the changes in organ and tissue levels, there are still lack of successful treatments for HFpEF given the complexity molecular networks remaining unknown. Here we report that the significantly changed genes of HFpEF rats associates positively with inflammatory processes and immune responses while negatively with calcium ion transport into cytosol. GSEA analysis shows several KEGG pathways are significantly enriched in HFpEF rats including p53 signaling pathway, Toll like receptor signaling pathway and so on. Our study provides new insights into HFpEF pathogenesis and a new therapeutic against HFpEF.
2019-02-05 | GSE126062 | GEO
Project description:Identification ofputative ClpXP substrates by combination of proteome analysis and TAILS N termini profiling from wt and ClpP-deficient mouse heart mitochondria, combined with substrate trapping using catalytically inactive ClpP expressed in MEF cell culture. This dataset provides the preTAILS proteomedata
2020-06-01 | PXD018194 | Pride
Project description:Mitochondria, the powerhouse of the cell, has been recognized as the key players in cancer cell biology, including cancer metabolism, metastasis, and drug resistance. Recent studies have demonstrated a functional interplay between mitochondria and epithelial-mesenchymal transition (EMT) in cancer. To delineate the role of mitochondrial components in this interplay, we induced the EMT in hepatoma HepG2 cells. Mitochondria was isolated from EMT-HepG2 cells, untreated HepG2 cells, and normal hepatic HL7702 cells. Mitochondrial RNAs were isolated for Illumina sequencing. Identification of mitochondrial RNAs that regulate EMT or mitochondria function may serve as potential therapeutic targets for developing new strategies to treat cancers.
2019-08-27 | GSE119946 | GEO
Project description:Dysfunctional Parkin-mediated mitophagic culling of senescent or damaged mitochondria is a major pathological process underlying Parkinson disease and a potential genetic mechanism of cardiomyopathy. Despite epidemiological associations between Parkinson disease and heart failure, the role of Parkin and mitophagic quality control in maintaining normal cardiac homeostasis is poorly understood.We used germline mutants and cardiac-specific RNA interference to interrogate Parkin regulation of cardiomyocyte mitochondria and examine functional crosstalk between mitophagy and mitochondrial dynamics in Drosophila heart tubes. 5 wild-type mouse hearts; 4 germline Parkin knockout mouse hearts Please note that the mouse cardiac examples were an adjunct to the Drosophila studies that comprised most of the associated publication. However, mRNA-sequencing was only performed on the mouse samples, not the Drosophila heart tubes.
2015-10-31 | E-GEOD-74517 | biostudies-arrayexpress
Project description:The goals of this study were to determine the effects of lateral transfer of mitochondria on recipient cell biology. We therefore collected cancer cells with and without macrophage mitochondria, and macrophages with and without cancer cell mitochondria, and analyzed transcriptomes by single-cell RNA-sequencing. Through our analysis, we found that cancer cells that received macrophage mitochondria have an enrichment of transcripts associated with cell cycle progression compared to cancer cells without macrophage mitochondria. We further validated these findings with wet lab experiments using cell proliferation markers.
2021-08-06 | GSE181410 | GEO
Project description:The mitochondrial mutator mouse is a well-established model of premature aging in which a progeroid phenotype is driven by the accumulation of somatic mtDNA mutations. Despite evidence of bioenergetic disruption within the cardiac mitochondria, there is little information about the underlying changes to the mitochondrial proteome. Herein, nLC-MS/MS was used to interrogate the mitochondria-enriched proteome of cardiac and skeletal muscle tissues of mutator mice and wild-type littermates. The mitochondrial proteome from heart tissue was then correlated with previously reported respiratory conductance data generated from the same mitochondrial samples to identify protein biomarkers of respiratory insufficiency. The majority of proteins that were found to be significantly downregulated in mutator mitochondria were subunits of respiratory complexes I and IV, including both nuclear and mitochondrial-encoded proteins. Interestingly, the mitochondrial-encoded complex V subunits, were unchanged or upregulated in mutator mitochondria suggesting a robustness to mtDNA mutation. Finally, the protein most strongly correlated with respiratory conductance in heart mitochondria from wild-type and mutator mice was the phosphatase PPM1K, which has been shown to have roles in branched chain amino acid metabolism and mitochondria permeability transition. These results suggest that mitochondrial mutator mice undergo a specific loss of mitochondrial complexes I and IV that limit their respiratory function independent of an upregulation of complex V. Additionally, the role of PPM1K in responding to mitochondrial stress warrants further exploration.
2021-01-08 | PXD017000 | JPOST Repository