Extracellular vesicles (Record no. 16313)

Metadata
000 -Etiqueta do registo
campo de controlo de comprimento fixo nam a22 4500
001 - Identificador do registo
Campo de controlo 16313
100 ## - Dados Gerais de Proc.
Dados gerais de processamento 20240103d2023 k||y0pory50 ba
101 ## - Língua da publicação
Língua do texto, banda sonora, etc. Inglês
102 ## - País de Publicação
País de publicação Portugal
200 ## - Título
Título próprio Extracellular vesicles
Informação de outro título communication agents in prediabetes
Primeira menção de responsabilidade Pedro Pereira
Outras menções de responsabilidade orient. Rita Oliveira, Maria Macedo
210 ## - Publicação, Distribuição
Lugar da edição, distribuição, etc. Lisboa
Nome do editor, distribuidor, etc. NOVA Medical School, Universidade NOVA de Lisboa
Data da publicação, distribuição, etc. 2023
215 ## - Descrição física
Descrição física 89 p.
Outras indicações físicas fig., tab.
328 ## - Nota de dissertação ou tese
Especificações da dissertação ou tese e tipo de grau académico Dissertação de Mestrado
Área cientifica do grau académico Investigação Biomédica
Ano do grau académico 2023
Instituição que confere o grau académico Faculdade de Ciências Médicas, Universidade NOVA de Lisboa
330 ## - Sumário ou Resumo
Texto da nota Diabetes entails numerous metabolic alterations across multiple organs, highlighting the critical role of inter-organ communication in its pathogenesis. Interestingly, extracellular vesicles (EVs) are agents of systemic communication, in both physiological and pathological contexts. Nevertheless, the intricate molecular mechanisms through which EVs operate in the context of diabetes remain unclear. Furthermore, plasma-derived extracellular vesicles (PDEVs) are increasingly recognized as pivotal mediators of inter-organ communication and potential sources of novel biomarkers for various medical conditions. To decipher the intricate messages encapsulated in EVs, under prediabetic conditions, we isolated PDEVs from diet induced prediabetic murine models. PDEVs presented mean size typical of small EVs, with no exclusive classification as exosomes due to the absence of intracellular origin analysis. Notably, prediabetic mice exhibited higher PDEV particle numbers and total protein concentrations, while average protein content per particle remained comparable between experimental groups. PDEVs proteomic profile unveiled a profound alteration in protein cargo under prediabetic conditions. Tandem mass spectrometry identified 5 proteins exclusively in HFD-PDEV, 112 exclusively in NCD-PDEV, and 223 shared across both groups. Prediabetes led to a decline in the diversity of PDEV protein cargo, suggesting a refined messaging system and more intense given that there are more circulating EVs in the prediabetic condition. Functional analysis of proteins exclusively identified in NCD-PDEV revealed significant enrichments in certain molecular functions, pointing to roles in protein folding, phosphatase activity, and hydrolase activity. The function of a protein is inherently linked to its conformation, and aberrations in protein folding give rise to a spectrum of cellular alterations associated with the etiology of various human diseases. These findings highlight the importance of proper folder in maintaining metabolic homeostasis. Noteworthy, the merely presence of a specific protein in the cell is insufficient for proper function, that is dependent on its post-translational modifications (PTMs). Next, we explored the PTMs within the identified proteins with a focus on acetylation and glycation. Intriguingly, prediabetic conditions correlated with an overall decreased acetylation and glycation events, indicating altered regulatory mechanisms in prediabetes. The gut plays a crucial role in regulating metabolism, and we have previously revealed that gut-derived extracellular vesicles (GDEVs) hold particular significance in the context of diabetes. Earlier we characterized the GDEV’ proteome. In this study, we revisit and expand upon our prior findings by analyzing the PTMs within GDEVs. Prediabetic conditions led to a decrease in both acetylation events, similar to the observations in PDEVs. Understanding the overlap between PDEVs and GDEVs is crucial in elucidating potential biomarkers and mechanisms underlying prediabetes. We identified four proteins exclusively present in the healthy state of both PDEVs and GDEVs, and the term "immune response" emerged as noteworthy. Hinting at immune regulation as pivotal in dysmetabolism. Importantly, their absence in prediabetes suggests their vital role in maintaining metabolic health. Complement Factor H, one of these proteins, has been associated with metabolic disorders. Additionally, overlapping iBAQ data between PDEVs and GDEVs identified four common proteins. Despite their shared presence, marked differences in fold change values between PDEVs and GDEVs precluded direct analogies or comparisons. This comprehensive exploration of proteomic alterations and PTMs in both PDEVs and GDEVs provides valuable insights into the intricate mechanisms underlying prediabetes, shedding light on potential biomarkers and pathways for future research
606 ## - Nome comum
Koha Internal code 22030
Elemento de entrada Extracellular Vesicles
606 ## - Nome comum
Koha Internal code 5752
Elemento de entrada Prediabetic State
606 ## - Nome comum
Koha Internal code 30
Elemento de entrada Academic Dissertation
700 ## - Responsabilidade principal
Koha Internal Code 24789
Palavra de ordem Pereira
Outra parte do nome Pedro Miguel Baptista
702 ## - Responsabilidade secundária
Código de função Orientador de tese
Koha Internal Code 24790
Palavra de ordem Oliveira
Outra parte do nome Rita Machado de
702 ## - Responsabilidade secundária
Código de função Orientador de tese
Koha Internal Code 24791
Palavra de ordem Macedo
Outra parte do nome Maria Paula
801 ## - Fonte de origem
País Portugal
Agência NMS
Regras de catalogação RPC
856 ## - Localização e acesso electrónico
URL http://hdl.handle.net/10362/161484
090 ## - Números de controlo do sistema (Koha)
Número biblioitem do Koha (gerado automaticamente) 16313
942 ## - Elementos de entrada adicionados (Koha)
Tipo de item no Koha Documento Eletrónico
Suprimido Disponível no OPAC
Holdings
Removido (estado) Perdido (estado) Data de aquisição Identificador de recurso uniforme Origem do registo (biblioteca) (codificado) Código da organização que empresta ou é detentora (biblioteca) Localização da prateleira Código de barras Cota Tipo de circulação (não pode ser emprestado) Tipo de item e material
Disponível Disponível 2024-01-03 http://hdl.handle.net/10362/161484 Biblioteca NMS|FCM Biblioteca NMS|FCM online 20240001 RUN Normal Documento Eletrónico