MARISA PASSARELLI
Projetos de Pesquisa
Unidades Organizacionais
Departamento de Clínica Médica, Faculdade de Medicina
LIM/10 - Laboratório de Lípides, Hospital das Clínicas, Faculdade de Medicina
LIM/10 - Laboratório de Lípides, Hospital das Clínicas, Faculdade de Medicina
3 resultados
Resultados de Busca
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- Novel Role of CETP in Macrophages: Reduction of Mitochondrial Oxidants Production and Modulation of Cell Immune-Metabolic Profile(2022) DORIGHELLO, Gabriel G.; ASSIS, Leandro H. P.; RENTZ, Thiago; MORARI, Joseane; SANTANA, Monique F. M.; PASSARELLI, Marisa; RIDGWAY, Neale D.; VERCESI, Anibal E.; OLIVEIRA, Helena C. F.Plasma cholesteryl ester transfer protein (CETP) activity diminishes HDL-cholesterol levels and thus may increase atherosclerosis risk. Experimental evidence suggests CETP may also exhibit anti-inflammatory properties, but local tissue-specific functions of CETP have not yet been clarified. Since oxidative stress and inflammation are major features of atherogenesis, we investigated whether CETP modulates macrophage oxidant production, inflammatory and metabolic profiles. Comparing macrophages from CETP-expressing transgenic mice and non-expressing littermates, we observed that CETP expression reduced mitochondrial superoxide anion production and H2O2 release, increased maximal mitochondrial respiration rates, and induced elongation of the mitochondrial network and expression of fusion-related genes (mitofusin-2 and OPA1). The expression of pro-inflammatory genes and phagocytic activity were diminished in CETP-expressing macrophages. In addition, CETP-expressing macrophages had less unesterified cholesterol under basal conditions and after exposure to oxidized LDL, as well as increased HDL-mediated cholesterol efflux. CETP knockdown in human THP1 cells increased unesterified cholesterol and abolished the effects on mitofusin-2 and TNF alpha. In summary, the expression of CETP in macrophages modulates mitochondrial structure and function to promote an intracellular antioxidant state and oxidative metabolism, attenuation of pro-inflammatory gene expression, reduced cholesterol accumulation, and phagocytosis. These localized functions of CETP may be relevant for the prevention of atherosclerosis and other inflammatory diseases.
- Aerobic Exercise Training Reduces Atherogenesis Induced by Low-Sodium Diet in LDL Receptor Knockout Mice(2022) BOCHI, Ana Paula Garcia; FERREIRA, Guilherme da Silva; BIANCO, Vanessa Del; PINTO, Paula Ramos; RODRIGUES, Leticia Gomes; TREVISANI, Mayara da Silva; FURUKAWA, Luzia Naoko Shinohara; BISPO, Kely Cristina Soares; SILVA, Alexandre Alves da; VELOSA, Ana Paula Pereira; NAKANDAKARE, Edna Regina; MACHADO, Ubiratan Fabres; TEODORO, Walcy Paganelli Rosolia; PASSARELLI, Marisa; CATANOZI, SergioThis study investigated the efficacy of aerobic exercise training (AET) in the prevention of dyslipidemia, insulin resistance (IR), and atherogenesis induced by severe low-sodium (LS) diet. LDL receptor knockout (LDLR KO) mice were fed a low-sodium (LS) (0.15% NaCl) or normal-sodium (NS; 1.27% NaCl) diet, submitted to AET in a treadmill, 5 times/week, 60 min/day, 15 m/min, for 90 days, or kept sedentary. Blood pressure (BP), plasma total cholesterol (TC) and triglyceride (TG) concentrations, lipoprotein profile, and insulin sensitivity were evaluated at the end of the AET protocol. Lipid infiltration, angiotensin II type 1 receptor (AT1), receptor for advanced glycation end products (RAGE), carboxymethyllysine (CML), and 4-hydroxynonenal (4-HNE) contents as well as gene expression were determined in the brachiocephalic trunk. BP and TC and gene expression were similar among groups. Compared to the NS diet, the LS diet increased vascular lipid infiltration, CML, RAGE, 4-HNE, plasma TG, LDL-cholesterol, and VLDL-TG. Conversely, the LS diet reduced vascular AT1 receptor, insulin sensitivity, HDL-cholesterol, and HDL-TG. AET prevented arterial lipid infiltration; increases in CML, RAGE, and 4-HNE contents; and reduced AT1 levels and improved LS-induced peripheral IR. The current study showed that AET counteracted the deleterious effects of chronic LS diet in an atherogenesis-prone model by ameliorating peripheral IR, lipid infiltration, CML, RAGE, 4-HNE, and AT1 receptor in the intima-media of the brachiocephalic trunk. These events occurred independently of the amelioration of plasma-lipid profile, which was negatively affected by the severe dietary-sodium restriction.
- Dietary Sodium and Nonalcoholic Fatty Liver Disease: A Systematic Review(2023) FERREIRA, Guilherme da Silva; CATANOZI, Sergio; PASSARELLI, Marisa(1) Introduction: Restriction in sodium intake is an important strategy for reducing cardiovascular morbidity and mortality, considering the direct influence of high-sodium diet consumption on the development of hypertension and cardiovascular diseases. There are only a few studies dealing with the influence of dietary sodium on the development of nonalcoholic fatty liver disease (NAFLD). In this systematic review, evidence in humans and animal models was compiled in a critical view of the influence of dietary sodium intake patterns on NAFLD markers; (2) Methods: Systematic review of PubMed data. Clinical outcomes included the prevalence/incidence of NAFLD for human studies, and NAFLD markers (hepatic lipogenesis, and markers of steatosis, fibrosis, and inflammation) for animal studies. The protocol was registered at the International Prospective Register of Systematic Review (PROSPERO; CRD42023390447); (3) Results and Conclusion: Seven studies in humans and eight in animals were included. All studies in humans were observational and associated high-sodium intake with NAFLD. However, in animals, both the increased and reduced consumption of sodium negatively influenced markers of liver steatosis, inflammation, and fibrosis.