Navegando por Palavras-chave "Lipid Rafts"

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    Influência Do Coacervado De Proteínas Do Soro Do Leite E Galactooligossacarídeo Na Resposta Inflamatória, Perfil Dos Fosfolipídeos E Microbiota Intestinal Em Camundongos Com Obesidade Induzida Por Dieta
    (Universidade Federal de São Paulo (UNIFESP), 2018-07-12) Amaral, Juliane Suzuki [UNIFESP]; Esposito, Elisa [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    Whey protein products such as Coacervate whey protein (Coa), galactooligosaccharide (Gos) and both associated (COAG) were tested in mice fed with a high fat diet to verify changes on enterocyte structural lipid profile, inflammation and intestinal microbiota composition during obesity. Males C57BL/6 were fed normolipid and high fat diets, divided into five experimental groups: 1) Normolipid control (Nwater), 2) High fat control (HFwater), 3) High fat + Coa (HFCoa), 4) High fat + Gos (HFGos) and 5) High fat Coa + Gos (HFCOAG), for 16 weeks treatment. Stool samples were collected at the end of the experiment and frozen in cryotubes for metagenomic analysis. The intestine was divided in: duodenum, cecum and colon, frozen in cryotubes until the processing data for cytokine dosage, evaluation of TLR4 protein and the main classes of fatty acid profile: phosphatidylcholine (PC), phosphatidylethanolamine (PE) and sphingomyelin (SM). The biometric data showed that HFCoa and HFCOAG groups maintained the same body mass gain as normolipid control, but only HFCOAG decreased adiposity and energy efficiency compared HFwater. The different diets changed the gut microbiota. Among treatments, the composition of the HFCOAG gut microbiota was closer to normolipid control group showing high percentages of dissimilarity for healthy state bacteria such as Lachnospiracea and Porphyromonas and the taxon RF39 as microbial signature. HFCoa group showed the best anti-inflamatory activity in the cecum (IL / 10 / TNFα). HFGos group decreased IL-1β with concomitant high levels of IFNγ, which correlated positively with Bilophila genus suggesting an influence of this taxon on IFNγ production. The percentage of vaccenic acid (18: 1n7) in the SM class of colon membrane increased in all treatments showing its possible relation with lipid raft instability on TLR4 activation. TLR4 receptors showed no difference in its expression, but changes on its activation is inferred since a decrease of the IL-6 was observed in this tissue. HFCOAG treatment increased vaccenic and myristoleic acid (14: 1n9) in SM class demonstrating correlations with an improvement of anti-inflammatory activity in colon. The increase of vaccenic acid was correlated to the Mogibacteriacea taxon. HFGos treatment increased palmitoleic acid (16: 1n7) in PC class, which was negatively correlated with an anti-inflammatory activity in colon. In general, there was a clear diet influence that directly promotes changes in gut microbiota profile and alters metabolic response during obesity as consequence. COAG showed the best preventive response among treatments in this research, but more studies are necessary to evaluate other metabolic aspects in different tissues and on the development of this compound that may be used as a prophylactic against obesity in the future.
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    Paracoccidioides brasiliensis induces recruitment of alpha 3 and alpha 5 integrins into epithelial cell membrane rafts, leading to cytokine secretion
    (Elsevier science bv, 2016) Barros, Bianca Carla Silva Campitelli de [UNIFESP]; Maza, Paloma Korehisa [UNIFESP]; Alcantara, Cristiane [UNIFESP]; Suzuki, Erika [UNIFESP]
    Paracoccidioides brasiliensis is one of the etiological agents of paracoccidioidomycosis, a human systemic mycosis, highly prevalent in Latin America. In the present work, we demonstrate that P. brasiliensis yeasts promote IL-6 and IL-8 secretion by the human lung epithelial cell line A549 in an integrin-dependent manner. In fact, small interfering RNA directed to alpha 3 and alpha 5 integrins decreased IL-6 and IL-8 levels in P. brasiliensis-infected A549 cell cultures. This fungus also led to an increase in the expression of alpha 3 and alpha 5 integrins in this epithelial cell line. In addition, P. brasiliensis yeasts promoted alpha 3 and alpha 5 integrins clustering into A549 cell membrane rafts. Furthermore, epithelial cell membrane raft disruption with nystatin decreased IL-6 and IL-8 levels in P. brasiliensis-A549 cell cultures. Therefore, by increasing host alpha 3 and alpha 5 integrins levels and clustering these receptors into membrane rafts, P. brasiliensis yeasts may modulate host inflammation. (C) 2015 Institut Pasteur. Published by Elsevier Masson SAS. All rights reserved.
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    Prnp/prion protein regulates the secretion of exosomes modulating cav1/caveolin-1-suppressed autophagy
    (Univ Federal Juiz Fora, Campus Univ, 2016) Dias, Marcos V. S.; Teixeira, Bianca L.; Rodrigues, Bruna R.; Sinigaglia-Coimbra, Rita [UNIFESP]; Porto-Carreiro, Isabel; Roffe, Martin; Hajj, Glaucia N. M.; Martins, Vilma R.
    Prion protein modulates many cellular functions including the secretion of trophic factors by astrocytes. Some of these factors are found in exosomes, which are formed within multivesicular bodies (MVBs) and secreted into the extracellular space to modulate cell-cell communication. The mechanisms underlying exosome biogenesis were not completely deciphered. Here, we demonstrate that primary cultures of astrocytes and fibroblasts from prnp-null mice secreted lower levels of exosomes than wild-type cells. Furthermore, prnp-null astrocytes exhibited reduced MVB formation and increased autophagosome formation. The reconstitution of PRNP expression at the cell membrane restored exosome secretion in PRNP-deficient astrocytes, whereas macroautophagy/autophagy inhibition via BECN1 depletion reestablished exosome release in these cells. Moreover, the PRNP octapeptide repeat domain was necessary to promote exosome secretion and to impair the formation of the CAV1-dependent ATG12-ATG5 cytoplasmic complex that drives autophagosome formation. Accordingly, higher levels of CAV1 were found in lipid raft domains instead of in the cytoplasm in prnp-null cells. Collectively, these findings demonstrate that PRNP supports CAV1-suppressed autophagy to protect MVBs from sequestration into phagophores, thus facilitating exosome secretion.