Examinando por Autor "Vecchiola, Andrea"
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Ítem Adipocyte extracellular vesicles (AdEVs) promote a proinflammatory and profibrotic profile in human renal and endothelial cells in vitro(Springer Nature, 2026-02-23) Carrión, Pablo; Hernández, María Paz; Pérez, Jorge A.; Tapia-Castillo, Alejandra; Vecchiola, Andrea; Sandoval-Bórquez, Alejandra; Baudrand, René F.; Fardella, Carlos E.; Carvajal, Cristian A.OBJECTIVES: In obesity, white adipose tissue (WAT) undergoes hypertrophic and hyperplastic changes that are driven by phenotypical changes in preadipocytes and adipocytes. WAT also causes a chronic inflammatory state that modifies gene expression and the secretome, including the shedding of adipose-derived extracellular vesicles (AdEVs) into the circulation, which may influence distant cell types and modulate their phenotypes. AIM: To evaluate the effects of AdEVs on renal and endothelial cells and determine their impact on gene expression related to inflammation, fibrosis, and endothelial function. METHODS: Human SW872 preadipocytes were differentiated into adipocytes and subsequently characterized. AdEVs were isolated by ultracentrifugation and analyzed according to ISEV guidelines. Recipient human renal (HCD) and endothelial (EA.hy926) cells were exposed to AdEVs for 24 hours. Gene expression of adipokines, cytokines (IL-6, IL-1B), fibrosis markers, neutrophil gelatinaseassociated lipocalin (NGAL), and eNOS was assessed by RT-qPCR and western blotting. RESULTS: Differentiated SW872 cells displayed typical adipocyte morphology and accumulated abundant lipid droplets. Isolated AdEVs showed a donut-like morphology, characteristic size distribution, and expression of CD9 and TSG101, consistent with canonical EV markers. Both renal and endothelial cells internalized PKH67-labeled AdEVs and exhibited increased IL-6 and IL-1B expression (p < 0.05). Renal cells demonstrated increased NGAL mRNA levels, whereas endothelial cells showed reduced eNOS mRNA expression following AdEV exposure (p < 0.05). CONCLUSION: AdEVs from SW872 upregulated cytokine (e.g., IL-6) and NGAL expression in renal cells, while reducing eNOS expression in endothelial cells. These findings suggest that AdEVs may influence early inflammatory and vascular responses inobesity.Ítem Primary Aldosteronism in a Hispanic Cohort: Responses to Mineralocorticoid Receptor Antagonism and Remission in a Case(Oxford University Press, 2025-02) Tapia-Castillo, Alejandra; Vecchiola, Andrea; Quiñones, Paola; Baudrand, René; Uslar, Thomas; Delgado, José; Carvajal, Cristian A.; Fardella, Carlos E.Background: Primary aldosteronism (PA) is the main cause of secondary arterial hypertension. In this study, we present the medical treatment of Hispanic patients with PA followed for up to 5 years, highlighting the complete cure with pharmacological treatment in one of our patients. Methods: We studied 32 PA patients, followed every 6 months after starting MRA. A clinical response was the normalization of blood pressure (BP) in the absence of other antihypertensive drugs. The biochemical response was considered with normalization of potassium and renin. Responses to treatment were compared using the defined daily dose (DDD). The effect of MRA was evaluated in vitro. The HAC15 cells were cultured and stimulated with aldosterone and spironolactone for 24-72 h, and the apoptotic cell death was measured. Results: At 12 months posttreatment with MRA, 68% of the patients had a total clinical response, and 67% had a total biochemical response. Response to MRA treatment reduced DDD by an average of 74%. Additionally, we observed one PA patient treated with spironolactone after 3 years, he presented a pharmacological cure with normalization of aldosterone and renin without treatment with spironolactone. The in vitro study shows that spironolactone increased early apoptosis by 60% and late apoptosis by 50%. Conclusions: These results suggest the importance of timely diagnosis of PA and specific treatment with MRA, especially in patients with a poor response to treatment. Moreover, remission of PA may occur in some patients after spironolactone treatment due to its suggestive role as an apoptotic agent.