Littérature scientifique sur le sujet « Vésicules extracellulaires, microARN »
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Thèses sur le sujet "Vésicules extracellulaires, microARN"
Lemaire, Quentin. « Étude des microARNs dans les vésicules extracellulaires microgliales : signatures et neuroprotection ». Thesis, Lille 1, 2019. http://www.theses.fr/2019LIL1S105/document.
Texte intégralIn the Central Nervous System (CNS), the glial cells influence neuronal activities. The microglial cells, resident immune cells of the CNS, greatly control the neuroinflammatory state. This control is particularly important in physiological functions and is often defective in neuropathologies. The microglial cell activities depend on the brain microenvironment and they communicate with other cell types (astrocytes, oligodendrocytes and neurons) to control the neuroinflammatory state. Among the different mechanisms of intercellular communication within the CNS, extracellular vesicles (EVs) play a major role in physiological processes (development, homeostasis, etc.) and pathological processes (neurodegenerative diseases, etc.). Therefore, this mode of communication was studied in the dialogue between microglia and neurons in the leech Hirudo medicinalis. This annelid is an interesting model of neurobiology thanks to the linear structure of its nervous system and the organization of its cell types. It allows the study of the dialogue between microglial cells and neurons at the level of an experimental lesion. At first, the results showed that microglial cells interact with neurons during CNS injury and that EVs are released at the level of this lesion. In addition, microglial cells produce EVs that interact with neurons and deliver a neurotrophic effect in vitro on leech and rat neurons. In a second step, the complexity of the vesicular compounds as well as efficiency requirements related to the isolation methods led us to develop the non-targeted proteomic analysis on a large scale in order to validate the positive EV fractions but also to identify their biologically active protein signatures. In a last part, we were interested in the microRNAs (miRNAs) contained in microglial EVs. The results allowed the identification of 6 miRNAs in microglial EVs, of which only one, miR-146a, is described to date in the mammalian CNS. In a context of neuroprotective dialogue between microglial EVs and neurons, the analysis of neuronal protein signatures predicted mRNAs potentially regulated by miRNAs contained in EVs. These 6 miRNAs were also identified in EVs derived from mouse, rat and human microglia. Overall, the results show that microglial cells in the leech produce EVs, exerting a neurotrophic effect on neurons, including rat neurons. The identification of the molecules present in these microglial EVs (proteins and miRNAs) made it possible to raise perspectives on the neuroprotective mechanisms supporting this microglia-neuron dialogue that will be interesting to examine in mammals in a context of nerve injury
Kervadec, Anaïs. « Évaluation des vésicules extracellulaires dérivées de cellules cardiaques humaines comme une alternative à la greffe des cellules : applications dans un modèle d'insuffisance cardiaque chronique ». Thesis, Sorbonne Paris Cité, 2017. http://www.theses.fr/2017USPCB015/document.
Texte intégralHeart failure (HF) is a major public health concern. The lack of donor hearts and the resistance of numerous patients to conventional treatments has led scientists to develop new therapies such as cell therapy. The initial goal of cell therapy was to repopulate the infarcted heart by directly injecting viable and functional cells. However, the rapid disappearance of the transplanted cells contrasts with their long term, ongoing functional benefits, suggesting that cells may act through a paracrine mechanism. Extracellular vesicles (EV), including exosomes and microparticles, may be key to this process, acting as shuttles to transport bioactive macromolecules that stimulate endogenous repair pathways in the host tissue. This PhD project demonstrates: 1) The non-inferiority of EV secreted by cardiovascular progenitors (Pg) derived from human embryonic stem cells as compared to their parent cells in a mouse model of chronic HF (CHF). These EV could act by the activation of endogenous signaling pathways implicated in cell proliferation, survival, DNA repair and decreased fibrosis. Their specific content, such as miRNA, could be involved in these benefits. 2) The importance of the cell type in the production of therapeutically effective EV, since EV derived from mature cardiomyocytes and mesenchymal stem cells did not improve cardiac function in mice with CHF. 3) The importance of EV in paracrine effects of cells, confirmed by the improvement of cardiac function in mice with CHF treated with EV secreted by Pg derived from iPS cells. In vitro data shows that EV might have pro-angiogenic, pro-proliferative and pro-survival effects. An acellular therapy should be clinically relevant by reducing technical, immunological and safety problems associated with cell transplantation. If this hypothesis is confirmed, regulatory concerns would be simplified and production costs reduced, facilitating large-scale production
Soula, Anaïs. « Rôle des microARNs cellulaires et vésiculaires dans la régulation transcriptomique du système nerveux ». Thesis, Bordeaux, 2017. http://www.theses.fr/2017BORD0794/document.
Texte intégralThis work consists in stuying the expression, the role and the transport of microRNAs (miRNAs) in the central nervous system (CNS). microRNAs (miRNAs) are small endogenous non coding RNAs, exerting a negative regulation on gene expression.They inhibit protein translation by hybridization on the 3’ untranslated region of mRNA.First, we have revealed the specific role of miR-92a in the control of the expressionof GluA1, in an homeostatic plasticity paradigm in which the synaptic plasticity is inhibited.Second, by using RNA-Seq technology, we showed that miRNAs are differentially expressed in the different structures of the CNS. Moreover, we have discovered new species of miRNAs. Finally, our results suggest that the miRNA expression (of known and new miRNAs) participate in the singular transcriptomique signature of each structure.Third, we have shown that miRNAs are transported into EVs, and can be exchanged between the cells of the CNS. The miRNA content of EVs varies depending on neuronal activity. Target prediction of these miRNAs includes genes involved in the regulation of neuronal plasticity. Together, our results suggest that the exchange of miRNAs through EVs is a new mechanism involved in the modulation of neuronal plasticity. Finally, we propose a new tool for purifiying EVs depending on their cellular origin.To conclude, this study allows a better understanding of the role of miRNAs in the regulation of the physiology of the CNS
Heliot, Amélie. « Étude de la réponse cellulaire et des Vésicules Extracellulaires produites par des macrophages primaires exposés aux particules fines (PM₂.₅) ». Thesis, Littoral, 2018. http://www.theses.fr/2018DUNK0522.
Texte intégralAir pollution is a major public health problem. In 2013, The International Agency for Research on Cancer classified air pollution and fine particle (PM₂.₅), with size lower than 2.5 µm, as carcinogenic to humans (group I). PM₂.₅ are able to penetrate deeply in lungs. When PM₂.₅ settle in pulmonary alveolar, they lead to strong inflammatory response, with inflammatory mediators ans extracellular vesicles release by infiltrating or resident immune cells. In this context, this thesis included two major aims : i) evaluate the physico-chemical characteristics of PM₂.₅ sampled in an industrial-urban site, identify their origin and study the seasonal variability of their composition ; ii) investigate the cellular response and EV produced by macrophages in response to PM₂.₅ and study EV's effects on epithelial cells. To achieve this, macrophages are exposed to PM₂.₅ collected in Dunkerque, and cellular response (oxidative stress, inflammation, polarization, miRNA) was quantified. EV released in response to PM₂.₅ exposition was isolated and characterized. Finally, epithelial cells, BEAS-2B, are exposed to EV released by exposed and non exposed macrophages to evaluate effects from this exposure (inflammation, oxidative stress, miRNA). We observed inflammation and anti-oxidant response in macrophages after PM₂.₅ exposure, as well as polarization modification. PM₂.₅ lead to increased number of EV by macrophages
Souki, Rima. « Utilisation des miARN circulants comme indicateurs d'exposition aux hydrocarbures aromatiques polycycliques seuls et en mélange ». Electronic Thesis or Diss., Université de Rennes (2023-....), 2023. http://www.theses.fr/2023URENB015.
Texte intégralPolycyclic Aromatic Hydrocarbons (PAH) are major environmental pollutants with toxic effects on human health. Among the cell types targeted by PAHs are circulating blood mononuclear cells (PBMC). The present study aims to 1) investigate the effect of B[a]P, a reference PAH, on the expression profile of microRNAs (miRNAs) in vitro in PBMCs, as well as in extracellular vesicles (EVs) secreted by these cells, using a small RNA-seq approach, 2) confirm the presence of vesicular miRNAs in vivo in the plasma of B[a]P-treated rats, 3) to analyze, by a bioinformatics approach, the potential targets of cellular and vesicular miRNAs and characterize, their signaling pathways and biological functions and 4) to understand the role of EVs and their miRNAs on the function and phenotype of adjacent endothelial cells. Our results identified B[a]P regulated miRNAs in PBMCs and ontology showed that their target genes were mainly involved in cell death and survival processes. Further studies revealed the importance of miR-132, which is regulated by B[a]P in a dose- and time-dependent manner, and require activation of the aryl hydrocarbon receptor (AhR). We also demonstrated that this miR-132 was involved in B[a]P-induced cell death by altering the balance of family 1 cytochrome P-450 (CYP), classically regulated by AhR. Our results then report an increase in EV release both in vitro from exposed PBMCs and in vivo in plasma from B[a]P-exposed rats and propose a panel of vesicular miRNAs regulated by PAH exposure. Finally, the ontological analysis revealed different miRNA expression profiles between PBMCs and their EVs, related to selective miRNA addressing within EVs. This last analysis led us to investigate the role of EVs from PBMCs after exposure to PAHs on neighboring endothelial cells. Our first results show internalization of these EVs is associated with a modification of the expression of endothelial genes involved in inflammation, oxidative stress, and migration. Altogether, these studies propose EVs and miRNAs as new tools not only to study the mechanisms of PAH toxicity but also to identify markers of exposure to these environmental pollutants
Giri, Khem. « Role of extracellular vesicles in type 1 diabetes ». Thesis, Nantes, Ecole nationale vétérinaire, 2020. http://www.theses.fr/2020ONIR136F.
Texte intégralType 1 diabetes (TlD) is an autoimmune disease that results from the destruction of insulin-secreting beta cells in the pancreas leading to chronic hyperglycaemia. Tl D arises early in life, as a result of a combination of genetic and environmental factors. Pro-inflammatory stimuli engender beta cell stress and apoptosis and release of autoantigens and danger-associated molecules priming the immune system. Extracellular vesicles (EV) are a heterogeneous population of membrane vesicles released by living cells. Based on their size, content and origin, EV are classified into apoptotic bodies (AB), microvesicles (MV) and small EV (sEV). As conveyors of biological active mate.rial, EV are involved in cell-to-cell communication. Evidence exists that beta cell sEV contribute to TlD pathogenesis, but the beneficial or detrimental immune properties of subtypes ofbeta EV generated under healthy or pathological conditions have not been compared yet. To this end, size-defined populations of EV were isolated from cell culture supematants of mouse insulinoma MIN6 beta cells exposed to proinflammatory cytokines associated with TlD (TNFα, IFNϒ, IL1β). Inflammatory stress increases the release of EV and enhances the export of the auto-antigen insulin in AB and sEV. Stress also favours packing of Toll-like receptor binding microRNA into sEV. These EV subpopulations differ in their aptitude to modulate dendritic cell (DC) activation and cytokine secretion from DC and RA W264.7 macrophages. By exploring the functional diversity of the beta EV repertoire, this work should help to elucidate the mechanisms underlying Tl D development and to identify new therapeutic targets
Yin, Min. « Vésicules extracellulaires et régulation de la réponse inflammatoire dans les pathologies cardiovasculaires ». Thesis, Sorbonne Paris Cité, 2015. http://www.theses.fr/2015PA05S009.
Texte intégralExtracellular vesicles, such as microvesicles and exosomes, are released during cell apoptosis or activation. They are important mediators of intercellular communication, suggesting that these vesicles could play a pathophysiological role, especially in cardiovascular diseases. Atherosclerosis is a chronic inflammatory disease of the arterial wall which results from the interaction between lipoproteins, inflammatory cells, and vascular cells. Myocardial infarction is an acute and severe complication of atherosclerosis. The postinfarction inflammatory response plays a central role in the formation of new blood vessels and scarring. However, the mechanisms of inflammation are still poorly known in these pathologies. My thesis concerned the effects of extracellular vesicles isolated from pathological tissues on inflammatory cells. We showed in the first work that microvesicles accumulating in human atherosclerotic lesions contribute to cholesterol and triglyceride overload in macrophages and facilitate foam cell formation. The accumulation of the intracellular lipids induced by those microvesicles is offset by an increase in cholesterol efflux associated with activation of ABCA1. In the second study, we examined the effect of vesicles produced in the infarcted heart on the inflammatory response. Our results showed : 1- an increased release in situ of microvesicles mostly of cardiomyocyte origin and exosomes 15 hours after infarction ; 2- the stimulation of monocyte VEGF production by extracellular vesicles ; 3- the incapacity of diabetic vesicles isolated from infarcted heart to reproduce that effect on control mice monocytes. In order to clarify the determinants of postischemic angiogenesis, we also studied miRNA profiles of control and diabetic vesicles. After myocardial infarction, the expression level of miR-126-3p and miR-92a-3p was significantly decreased in diabetic vesicles compared to control vesicles. Furthermore, we observed an increased expression of miR-126-3p and miR-92a-3p respectively in the microvesicles and the exosomes isolated from control mice heart after myocardial infarction. In conclusion, this work provides new information on the functions of extracellular vesicles locally generated in inflamed tissues, particularly in promoting macrophage transformation into foam cells in the atherosclerotic plaque. Furthermore, vesicles isolated from ischemic heart could enhance postinfarction angiogenesis by stimulating monocyte VEGF production. The loss of this beneficial effect in diabetes may be associated with changes of miRNA cargo in extracellular vesicles in this pathology