Proteomic analysis of extracellular vesicles and cells
Ontology highlight
ABSTRACT:
INSTRUMENT(S):
ORGANISM(S): Mus Musculus (mouse)
TISSUE(S): Primary Cell Line Cell
DISEASE(S): Disease Free
SUBMITTER: 
Adriana Franco Paes Leme
LAB HEAD: Adriana Franco Paes Leme
PROVIDER: PXD023259 | Pride | 2023-07-20
REPOSITORIES: Pride
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| 01dez_PatriciaRocco_Evs_10.raw | Raw | |||
| 01dez_PatriciaRocco_Evs_12.raw | Raw | |||
| 01dez_PatriciaRocco_Evs_16.raw | Raw | |||
| 01dez_PatriciaRocco_Evs_17.raw | Raw | |||
| 01dez_PatriciaRocco_Evs_6.raw | Raw |
Items per page: 5 1 - 5 of 20 |
Publications
Extracellular Vesicles from Different Sources of Mesenchymal Stromal Cells Have Distinct Effects on Lung and Distal Organs in Experimental Sepsis.
Blanco Natália G NG Machado Natália M NM Castro Ligia L LL Antunes Mariana A MA Takiya Christina M CM Trugilho Monique R O MRO Silva Luana R LR Paes Leme Adriana F AF Domingues Romênia R RR Pauletti Bianca A BA Miranda Beatriz T BT Silva Johnatas D JD Dos Santos Claudia C CC Silva Pedro L PL Rocco Patricia R M PRM Cruz Fernanda F FF
International journal of molecular sciences 20230504 9
The effects of the administration of mesenchymal stromal cells (MSC) may vary according to the source. We hypothesized that MSC-derived extracellular vesicles (EVs) obtained from bone marrow (BM), adipose (AD), or lung (L) tissues may also lead to different effects in sepsis. We profiled the proteome from EVs as a first step toward understanding their mechanisms of action. Polymicrobial sepsis was induced in C57BL/6 mice by cecal ligation and puncture (SEPSIS) and SHAM (control) animals only und ...[more]
Similar Datasets
Project description:A vast portion of the mammalian genome is transcribed as long non-coding RNAs (lncRNAs) acting in the cytoplasm with largely unknown functions. Surprisingly, lncRNAs have been shown to interact with ribosomes, encode uncharacterized proteins, or act as ribosome sponges. These functions still remain mostly undetected and understudied owing to the lack of efficient tools for genome-wide simultaneous identification of ribosome-associated lncRNAs and peptide-producing lncRNAs. Here we present AHARIBO, a method for the detection of lncRNAs either untranslated, but associated with ribosomes, or encoding small peptides. Using AHARIBO in mouse embryonic stem cells during neuronal differentiation, we isolated ribosome-protected RNA fragments, translated RNAs and corresponding de novo synthesized polypeptides. Besides identifying mRNAs under active translation and associated ribosomes, we found and distinguished lncRNAs acting as ribosome sponges or encoding micropeptides, laying the ground for a better functional understanding of hundreds lncRNAs.
2021-09-09 | PXD022679 | Pride
Project description:Osteoarthritis (OA) is a multifactorial pathology which comprises a wide range of distinct phenotypes. The characterization of the different molecular profiles associated to each phenotype can improve the classification of OA for a better personalized medicine. Within the metabolic syndrome phenotype, OA can co-exist with type 2 diabetes (TD2) disease. This study was undertaken to investigate lipidomic and proteomic differences between human OA and OA/TD2 cartilage through a multimodal mass spectrometry approach.
2021-04-20 | PXD021487 | Pride
Project description:The crucial role of nutrition for cerebral health and the impact of dietary habits on brain structure and function have been long far recognized. To date a major health concern is associated with the increased consumption of fructose as added sugar in many types of drinks and processed foods, especially among young people. High-fructose intake has been pointed out as the possible culprit for the raised incidence of chronic diseases, such as obesity, cardiovascular disease, nonalcoholic fatty liver disease, and type 2 diabete. Further, it has been reported that high-fructose intake is associated with the over-activation of its cerebral metabolism, which was proposed to negatively impact on whole brain physiology and cognitive function. Notably, we previously reported that short-term fructose-rich diet induces mitochondrial dysfunction, oxidative stress, and neuroinflammation in hippocampus of young rats, as well as the imbalance of redox homeostasis, autophagic mechanisms and representation of synaptic markers in frontal cortex of both adult and young rats. Animal studies have also revealed the damaging effect of high-fructose diets on hippocampal functions during periods of neurocognitive development, such as childhood and adolescence. Hypothalamus plays a crucial role in maintaining whole body homeostasis. Long-term fructose overfeeding was reported to alter hypothalamic-pituitary-adrenal axis, leading to elevations in glucocorticoids in peri-adolescent rats [22]. Further, fructose overconsumption was associated with impairment of hypothalamic insulin signalling, oxidative stress and inflammation , and it was proposed that fructose-driven perturbations of hypothalamic function may compromise the potential for satiety, thereby increasing the prospect of developing obesity. Data currently available on hypothalamic dysfunctions related to a high-fructose diet essentially refer to the effects of long-term sugar feeding, while information on corresponding alterations associated with a short-term dietary treatment, particularly in the critical period of adolescence, is still lacking. Due to complexity and multiplicity of hypothalamic functions, there is also the need for a holistic characterization aimed at unveiling the general picture of hypothalamic dysfunctions associated with a high-fructose diet. To fill this gap, we investigated adolescent rats fed a fructose-rich or control diet, for 3 weeks. To verify whether the fructose-driven changes are rescued after the switch to a control diet, half of the rats from both animal groups were then fed a control diet for additional 3 weeks until young adulthood phase. Quantitative proteomics on hypothalamic extracts of all animal groups was used to identify molecular alterations triggered by fructose-rich diet and to obtain insights into the relationship between sugar feeding and possible dysfunctions of hypothalamus.
2023-03-11 | PXD038834 | Pride
Project description:Non-alcoholic fatty liver disease (NAFLD) is the most prevalent liver pathology worldwide and is intimately linked with obesity and type 2 diabetes. Liver inflammation is a hallmark of NAFLD and is thought to contribute to tissue fibrosis and disease pathogenesis. Uncoupling protein 1 (UCP1) is exclusively expressed in brown and beige adipocytes and has been extensively studied for its capacity to elevate thermogenesis and reverse obesity. Here we identify an endocrine pathway regulated by UCP1 that antagonizes liver inflammation and pathology, independent of effects on obesity. We show that, without UCP1, brown and beige fat exhibit a diminished capacity to clear succinate from the circulation. Moreover, UCP1KO mice exhibit elevated extracellular succinate in liver tissue that drives inflammation through ligation of its cognate receptor succinate receptor 1 (SUCNR1) in liver-resident stellate cell and macrophage populations. Conversely, increasing brown and beige adipocyte content in mice antagonizes SUCNR1-dependent inflammatory signaling in the liver. We show that this UCP1-succinate-SUCNR1 axis is necessary to regulate liver immune cell infiltration and pathology, and systemic glucose intolerance in an obesogenic environment. As such, the therapeutic utility of brown and beige adipocytes, and UCP1, extends beyond thermogenesis and may be leveraged to antagonize NAFLD and SUCNR1-dependent liver inflammation.
2022-02-17 | PXD024717 | Pride
Project description:Entry into mitosis is driven by the coordinated phosphorylation of thousands of proteins. For the cell to complete mitosis and divide into two identical daughter cells it must regulate dephosphorylation of these proteins in a highly ordered, temporal manner. There is currently a lack of a complete understanding of the phosphorylation changes that occur during the initial stages of mitotic exit in human cells. Therefore, we performed a large unbiased, global analysis to map the very first dephosphorylation events that occur as cells exit mitosis. We identified and quantified the modification of >16,000 phosphosites on >3,300 unique proteins during early mitotic exit, providing up to 8-fold greater resolution than previous studies. Only a small fraction (~10%) of phosphorylation sites were dephosphorylated during early mitotic exit and these occurred on proteins involved in critical early exit events, including organization of the mitotic spindle, the spindle assembly checkpoint, and reformation of the nuclear envelope. Surprisingly this enrichment was observed across all kinase consensus motifs, indicating that it is independent of the upstream phosphorylating kinase. Therefore, dephosphorylation of these sites is likely determined by the specificity of phosphatase/s rather than the activity of kinase/s. Dephosphorylation was significantly affected by the amino acids at and surrounding the phosphorylation site, with several unique evolutionarily conserved amino acids correlating strongly with phosphorylation status. These data provide a potential mechanism for the specificity of phosphatases, and how they co-ordinate the ordered events of mitotic exit. In summary, our results provide a global overview of the phosphorylation changes that occur during the very first stages of mitotic exit, providing novel mechanistic insight into how phosphatase/s specifically regulate this critical transition.
2015-06-25 | PXD001559 | Pride
Project description:Mitochondrial Rho-GTPase (Miro), a protein found on the outer mitochondrial membrane, is required for mitochondrial transport, mitochondrial dynamics, and mitochondrial Ca2+ homeostasis. We previously reported that Miro2 plays a role in the survival of hippocampal neural stem (HCN) cells, with effects on mitochondrial morphology and function. Furthermore, we revealed that Miro2 expression level is associated with neurodegeneration in animal models of Alzheimer's disease and patients with dementia. Nevertheless, a comprehensive investigation is still needed; thus, we analyzed the interacting proteins of Miro2 to elucidate its mechanisms in HCN cells by employing TurboID-based proximity labeling.
2026-02-23 | PXD055479 | Pride
Project description:A standardized extract of Centella asiatica (ECa 233) strengthened the hippocampal synapses, resulting in the memory-enhancing effect. The ratio of the major active compounds in the extract – madecassoside [MDS] and asiaticoside [ASS] – is at 1.5 ± 0.5:1. However, the interactions between MDS and ASS are still unknown. To delineate the role of MDS and ASS in ECa 233 on synaptic enhancement by mimicking the applied MDS and ASS concentrations in ECa 233. The hippocampal slices obtained from healthy 8-week-old male Wistar rats and differentiated SH-SY5Y cells were treated with DMSO, ECa 233, MDS, ASS, or MDS+ASS. The hippocampal long-term potentiation (LTP was monitored for 3 h. The cell extracted proteins were examined by proteomic analysis. ECa 233 demonstrated the highest hippocampal synaptic response, followed by the MDS+ASS and the MDS, which expressed a stronger synaptic enhancement effect than the ASS. A number of mitochondrial proteins, including NDUFB6, were also expressed in the differentiated SH-SY5Y cells after treatment with ECa 233, ASS, MDS, and MDS+ASS. Our data revealed that the synergistic effect of MDS and ASS in the combined treatment was necessary to achieve the same level of responses obtained from ECa 233 treatment. MDS majorly contributed to the synaptic enhancement action of ECa 233. In addition, all substances were involved in mitochondrial metabolism, a process necessary for providing energy and sustaining synaptic Ca2+ levels in synaptic transmission. This discovery is crucial for dementia drug development because it demonstrated the role of major parent compounds in ECa 233 and their interaction.
2025-08-13 | PXD057572 | Pride
Project description:K-ras mutations are observed in around 40% human colorectal adenomas and carcinomas and contribute to the pathogenesis of human and rodent colorectal tumour formation. Previously, we developed and characterised a strain of transgenic mice with inducible intestinal epithelial expression of K-rasVal12 via a Cre/LoxP system. To evaluate the influence of mutant K-ras on carcinogen-induced colorectal tumourigenesis, we induced neoplastic alterations in the large intestines of wild-type and K-rasVal12 mice using the colon-selective carcinogen 1, 2-dimethylhydrazine (DMH), which has been widely used to study chemically induced colorectal tumours that are histopathologically similar to those observed in humans. K-rasVal12 expression significantly promoted DMH-induced colorectal tumourigenesis: the average life span of the mice decreased from 38.52±1.97 weeks for 40 wild-type mice to 32.42±2.17 weeks for 26 K-rasVal12 mice (mean+SEM, P<0.05) and the large intestinal tumours increased from 2.27±0.15 per wild-type mouse to 3.85±0.20 in K-rasVal12 mice (mean+SEM, P<0.01). Adenomas from DMH-treated K-rasVal12 mice showed significantly higher levels (10.9±1.69%) of Ki-67-positive proliferating cells compared with those from DMH-treated wild-type mice (7.77±1.15%) (mean+SD, P<0.01) and a mild increase in apoptotic nuclei staining for cleaved caspase-3 (1.94+0.51% compared with 1.15±0.34%, mean+SD, P<0.01). In the adenomas from DMH-treated K-rasVal12 mice, K-rasVal12 transgene recombination and expression were confirmed and shown to promote strong Erk and mild Akt activation compared with adenomas from DMH-treated wild-type mice. Microarray hybridization and cluster analysis demonstrated different expression profiles in adenomas from DMH-treated wild-type and DMH-treated K-rasVal12 mice, indicating involvement of different molecular mechanisms, but array-comparative genomic hybridisation analysis showed chromosome stability in both, with very few chromosome alterations observed in adenomas from either of the two groups. Taken together, these data show that mutant K-ras promotes DMH-induced colorectal tumourigenesis, conferring a proliferative effect, but does not alter chromosome stability in the tumours. This study has 7 samples analysed, 4 Kras mutants and 3 controls, on the Illumina Mouse-6 Beadchip array.
2010-10-02 | E-GEOD-24010 | biostudies-arrayexpress
Project description:Background Extracellular vesicles (EVs) secreted by mesenchymal stromal cells (MSCs) provide significant protection against renal ischemia-reperfusion injury (IRI). Hypoxia is considered an important method for enhancing the tissue repair capabilities of MSCs. However, the specific effects of hypoxia on MSCs and MSC-EVs, as well as their therapeutic potential for renal IRI, remain unclear. In this study, we investigated the alterations in MSCs and the production of MSC-EVs following hypoxia pre-treatment, and further explored the key intrinsic mechanisms by which hypoxic MSC-EVs treat renal IRI. Methods Human umbilical cord MSCs were cultured under normoxic and hypoxic conditions. Proliferation and related pathways were measured, and RNA sequencing was used to detect changes in the transcription profile. MSC-EVs from both normoxic and hypoxic conditions were isolated and characterized. In vivo, the localization and therapeutic effects of MSC-EVs were assessed in a rat renal IRI model. Histological examinations were employed to assess the structure, proliferation, and apoptosis of IRI kidney tissue respectively. Renal function was measured by analyzing serum creatinine and blood urea nitrogen levels. In vitro, the therapeutic potential of MSC-EVs were measured in renal tubular epithelial cells injured by antimycin A. Protein sequencing analysis of hypoxic MSC-EVs was conducted, and the depletion of Glutathione S-Transferase Omega 1 (GSTO1) in hypoxic MSC-EVs was performed to verify its key role in alleviating renal injury. Results Hypoxia alters MSCs transcription, promotes their proliferation, and increases the production of EVs. Hypoxia-pretreated MSC-EVs exhibited a superior ability to mitigate renal IRI, enhancing proliferation and reducing apoptosis of renal tubular epithelial cells both in vivo and in vitro. Protein profiling of the EVs revealed an accumulation of numerous anti-oxidative stress proteins, with GSTO1 being particularly prominent. GSTO1 knock down was significantly reduced the antioxidant and therapeutic effects in renal IRI of hypoxic MSC-EVs. Conclusions Hypoxia significantly promotes MSC-EVs generation and enhances the therapeutic effect of EVs on renal IRI. The effect of antioxidant stress induced by GSTO1 is one of the most important underlying mechanisms. Our findings underscore that hypoxia-pretreated MSC-EVs represent a novel and promising therapeutic intervention for renal IRI.
2025-05-07 | PXD057088 | Pride
Project description:Qualitative analysis of proteome is to study the types and quantities of proteome identified by samples under different conditions, and to perform functional analysis of the identified proteins, so as to provide reference information for quantitative and modification analysis of high-throughput proteins.In order to explore how USP20 plays a role in T-ALL through deubiquitination, we investigated the substrate protein of USP0 by protein determination spectrometry.
2025-10-13 | PXD053080 | Pride